(Facet) Joint Pain - pain

Transcription

Anesthesiology 2007; 106:591– 614
Copyright © 2007, the American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc.
Pathogenesis, Diagnosis, and Treatment of Lumbar
Zygapophysial (Facet) Joint Pain
Steven P. Cohen, M.D.,* Srinivasa N. Raja, M.D.†
l-z joint pain is defined in a functional capacity as pain
originating from any structure integral to both the function and configuration of the lumbar facet joints, including the fibrous capsule, synovial membrane, hyaline cartilage surfaces, and bony articulations.
A critical issue that must be addressed before embarking on any review of l-z joint pain is whether pain can be
definitively attributed to these joints. In the 1960s and
1970s, this question posed a legitimate controversy that
was vigorously debated in the medical literature.2,3 However, in the past 20 yr, the scales of this controversy have
resolutely tipped toward the conviction that l-z joints
can be and often are a primary source of low back pain
(LBP).4
Compelling evidence underlies this paradigmatic shift
in thinking. The facet joint capsule and surrounding
structures are richly imbued with nociceptors that fire
when the capsule is stretched or subjected to local
compressive forces.5,6 In both pain patients and volunteers, chemical or mechanical stimulation of the facet
joints and their nerve supply has been shown to elicit
back and/or leg pain.7–10 During spine surgery performed under local anesthetic (LA), lumbar facet capsule
stimulation elicits significant pain in approximately 20%
of patients.11 Last and most significantly, LA blocks of
either the facet joints themselves or the medial branches
innervating them have been shown to relieve pain in a
substantial percentage of patients with chronic LBP.12
Therefore, like other synovial joints in the human body,
the l-z joints represent a potential pain generator in
patients with chronic LBP.
In light of the prevalence of lumbar facet joint pain and
the frequency with which facet blocks are performed,
several reviews have been undertaken on this phenomenon in the past 15 yr. Although some of these articles
provided keen insight on various aspects of the condition, most were limited by their confined scope and
specialized target audiences. The purpose of this review
is therefore to provide a comprehensive, evidence-based
framework on the anatomy, pathophysiology, prevalence, diagnosis, and treatment of lumbar facet pain.
Articles reviewed were obtained via MEDLINE and Ovid
search engines, books and book chapters, and bibliographic references dating to the early 1900s.
This article has been selected for the Anesthesiology
CME Program. After reading the article, go to http://
www.asahq.org/journal-cme to take the test and apply for
Category 1 credit. Complete instructions may be found in
the CME section at the back of this issue.
Lumbar zygapophysial joint arthropathy is a challenging
condition affecting up to 15% of patients with chronic low back
pain. The onset of lumbar facet joint pain is usually insidious,
with predisposing factors including spondylolisthesis, degenerative disc pathology, and old age. Despite previous reports of a
“facet syndrome,” the existing literature does not support the
use of historic or physical examination findings to diagnose
lumbar zygapophysial joint pain. The most accepted method for
diagnosing pain arising from the lumbar facet joints is with
low-volume intraarticular or medial branch blocks, both of
which are associated with high false-positive rates. Standard
treatment modalities for lumbar zygapophysial joint pain include intraarticular steroid injections and radiofrequency denervation of the medial branches innervating the joints, but the
evidence supporting both of these is conflicting. In this article,
the authors provide a comprehensive review of the anatomy,
biomechanics, and function of the lumbar zygapophysial joints,
along with a systematic analysis of the diagnosis and treatment
of facet joint pain.
SINCE its original description almost 100 yr ago, thousands of scientific articles have been published on lumbar zygapophysial (l-z) joint pain, and facet interventions
represent the second most common type of procedure
performed in pain management centers throughout the
United States.1 But despite the plethora of research and
clinical emphasis on this disorder, almost every aspect of
l-z joint pain, from diagnosis to treatment, remains mired
in controversy. Even among pain specialists, lumbar
facet joint pain remains a misunderstood, misdiagnosed,
and improperly treated medical condition. In this article,
* Associate Professor, Department of Anesthesiology and Critical Care Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland, and Walter Reed
Army Medical Center, Washington, D.C. † Professor, Department of Anesthesiology and Critical Care Medicine and Department of Neurology, Johns Hopkins
School of Medicine.
Received from the Pain Management Division, Department of Anesthesiology
and Critical Care Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland. Submitted for publication May 16, 2006. Accepted for publication October
24, 2006. The opinions or assertions contained herein are the private views of the
authors and are not to be construed as official or as reflecting the views of the
Department of the Army or the Department of Defense. Dr. Cohen receives
partial salary support from the John P. Murtha Neuroscience and Pain Institute,
Johnstown, Pennsylvania, and the US Army. Dr. Raja has unrestricted grants from
Allergan (Irvine, California) and Ortho-McNeil (Raritan, New Jersey), and serves
as scientific advisor for Fralex Therapeutics (Toronto, Ontario, Canada). He
receives salary support from grant No. NS-26363 from the National Institutes of
Health, Bethesda, Maryland.
Historic Review
The l-z joints, often referred to as facet joints, have
long been recognized as a potential source of LBP. In
1911, Goldthwaite13 first noted that the peculiarities of
Address correspondence to Dr. Cohen: Division of Pain Medicine, Johns
Hopkins School of Medicine, 550 North Broadway, Suite 301, Baltimore, Maryland 21205. [email protected]. Individual article reprints may be accessed at
no charge through the Journal Web site, www.anesthesiology.org.
Anesthesiology, V 106, No 3, Mar 2007
591
592
the facet joints could be a significant source of back pain
and instability. Sixteen years later, after anatomical dissections of 75 cadavers, Putti14 suggested that local inflammation and degenerative changes in lumbar facet
joints could result in sciatica from irritation of nerve
roots. In 1933, Ghormley15 coined the term “facet syndrome,” which he defined as lumbosacral pain, with or
without sciatica, that was likely to occur after a sudden
rotatory strain. Shortly thereafter, interest in the l-z joints
as potential sources of back pain waned after the landmark article by Mixter and Barr16 implicating lumbar disc
rupture as the major cause of low back and leg pain. The
1940s saw a resurgence in the interest of l-z joints as pain
generators when Badgley17 suggested that up to 80% of
cases of LBP and sciatica are due to referred pain from l-z
joint pathology, rather than direct nerve root compression. In 1963, Hirsch et al.7 published the first account
whereby the injection of l-z joints reproduced patients’
back pain. Rees,18 who reported a success rate of 99.8%,
is generally credited with promoting percutaneous
“facet rhizolysis” with his ground-breaking report in the
early 1970s. Later, it was shown that the technique
advocated by Rees may not have been sufficient to
achieve rhizotomy in most patients.3 Buoyed by a high
incidence of hemorrhagic complications, Shealy19,20 pioneered the use of fluoroscopically guided radiofrequency facet denervation to treat l-z joint pain in the
mid-1970s.
S. P. COHEN AND S. N. RAJA
spectively. The medial branches of L1–L4 dorsal rami
course across the top of their respective transverse processes one level below the named spinal nerve (e.g., L4
crosses the transverse process of L5), traversing the
dorsal leaf of the intertransverse ligament at the base of
the transverse process. Each nerve then runs downward
along the junction of the transverse and superior articular processes, passing beneath the mamilloaccessory ligament and dividing into multiple branches as it crosses
the vertebral lamina (fig. 1). In some cases, the mamilloaccessory ligament becomes calcified, which may lead
to nerve entrapment.27 This is most common at L5 (approximately 20%) but also occurs at L4 (10%) and L3
(4%). In addition to two l-z joints, the medial branches
also innervate the multifidus muscle, the interspinous
muscle and ligament, and the periosteum of the neural
arch.7,28 –30 The L5 nerve differs in that it is the dorsal
ramus itself that runs along the junction of the sacral ala
and superior articular process of the sacrum.29,31 Its
medial branch arises opposite the inferolateral corner of
the base of the lowest facet joint. At this level, it is the
dorsal ramus rather than its medial branch that is amenable to blockade.
Some people may have aberrant or additional innervation of the facet joints. In a study conducted in asymptomatic volunteers, Kaplan et al.32 found that 1 in 9
subjects who underwent L4 –L5 (n ⫽ 5) and L5–S1 (n ⫽
4) facet joint medial branch blocks (MBB) felt pain dur-
Anatomy and Innervation
The lumbar facet joints form the posterolateral articulations connecting the vertebral arch of one vertebra to
the arch of the adjacent vertebra. As true synovial joints,
each facet joint contains a distinct joint space capable of
accommodating between 1 and 1.5 ml of fluid, a synovial
membrane, hyaline cartilage surfaces, and a fibrous capsule.21 The fibrous capsule of the lumbar facet joint is
approximately 1 mm thick and composed mostly of
collagenous tissue arranged in a more or less transverse
fashion to provide maximum resistance to flexion.22,23
The joint capsule is thick posteriorly, supported by fibers arising from the multifidus muscle. Superiorly and
inferiorly, the capsule attaches further away from the
osteochondral margins, forming subcapsular recesses
that in the normal joint are filled with fibroadipose menisci. Anteriorly, the fibrous capsule is replaced by the
ligamentum flavum.24
Each facet joint receives dual innervation from medial
branches arising from posterior primary rami at the same
level and one level above the z-joint.25,26 For example,
the inferior pole of the L4 –L5 facet joint receives innervation from the L4 medial branch and its superior pole is
innervated by the L3 medial branch, which are typically
blocked on the transverse processes of L5 and L4, reAnesthesiology, V 106, No 3, Mar 2007
Fig. 1. Right lateral oblique view of the lumbar vertebral bodies
and the dorsal rami medial branches. Drawing by Frank M.
Cort, M.S. (Research Associate, Department of Radiology, Johns
Hopkins Hospital, Baltimore, Maryland).
LUMBAR FACET JOINT PAIN
ing repeated capsular distension concordant with pain
experienced during previous l-z joint provocation without MBB. Assuming the blocks were technically successful, one explanation for this finding is that in a small
subset of individuals, aberrant innervation may account
for false-negative diagnostic MBB. Some authors have
suggested that l-z joints may also receive innervation
from the medial branch below the joint (i.e., S1 for the
L5–S1 joint),33,34 the dorsal root ganglion,35 and the
paravertebral sympathetic ganglia,36,37 but these assertions remain unproven (fig. 2).
Histologic studies have demonstrated that the lumbar
facet joints are richly innervated with encapsulated
(Ruffini-type endings, pacinian corpuscles), unencapsulated, and free nerve endings.5 The presence of low-threshold, rapidly adapting mechanosensitive neurons suggests
that in addition to transmitting nociceptive information,
the l-z facet capsule also serves a proprioceptive function.
Besides substance P and calcitonin gene–related peptide, a
substantial percentage of nerve endings in facet capsules
have also been found containing neuropeptide Y, indicating the presence of sympathetic efferent fibers.38,39 Nerve
fibers have also been found in subchondral bone and intraarticular inclusions of l-z joints, signifying that facet-mediated pain may originate in structures besides the joint
capsule.40 – 42 In degenerative lumbar spinal disorders, inflammatory mediators such as prostaglandins43 and the
inflammatory cytokines interleukin 1␤, interleukin 6, and
tumor necrosis factor ␣44 have been found in facet joint
cartilage and synovial tissue.
Function and Biomechanics
The basic anatomical unit of the spine, often referred
to as the three-joint complex, consists of the paired
Fig. 2. Schematic drawing of the spinal
cord and segmental spinal innervation.
Drawing by Specialist Frank and Angela
Dill, US Army, and Frank M. Cort, M.S.
(Research Associate, Department of Radiology, Johns Hopkins Hospital, Baltimore, Maryland).
593
zygapophysial joints and the intervertebral disc. Together, these joints function to support and stabilize the
spine, and prevent injury by limiting motion in all planes
of movement. Macroscopically, each facet joint is composed of a posteromedially facing concave superior articular process from the inferior vertebral body, and a
smaller anterolaterally facing inferior articular process
from the superior spinal level. The shape and orientation
of the l-z joints determine the role each plays in protecting the spine against excessive motion. Facet joints oriented parallel to the sagittal plane provide substantial
resistance to axial rotation but minimal resistance to
shearing forces (backward and forward sliding), whereas
joints oriented more in a coronal plane tend to protect
against flexion and shearing forces but provide minimal
protection against rotation (fig. 3).24 In an anatomical
study published in 1940 by Horwitz and Smith,45 the
authors found that the L4 –L5 z-joints tended to be more
coronally positioned (almost 70° with respect to the
sagittal plane), whereas the L2–L3 and L3–L4 joints were
likely to be oriented more parallel (⬍ 40°) to the sagittal
plane. In more recent studies by Masharawi et al.46 and
Punjabi et al.,47 the investigators found that the upper
lumbar facet joints (T12–L2) were oriented closer to the
midsagittal plane of the vertebral body (mean range,
26°–34°), whereas the lower facet joints tended to be
oriented away from that plane (40°–56°). In the upper
lumbar spine, approximately 80% of the facet joints are
curved, and 20% are flat. In the lower lumbar spine,
these numbers are reversed.45 Studies by Grobler et al.48
and Boden et al.49 found a positive association between
degenerative spondylolisthesis and more sagittally oriented lower lumbar facet joints.
In young people, the l-z joints are quite strong, capable
594
rior tip of the facets bottomed against the laminae
below, functioning as pivots for the entire vertebral
body to rotate backward. This resulted in considerable
stretching of the superior facet capsules, manifesting
as blood extravasating onto the outer surface of the
capsule. In another cadaveric study, Adams and Hutton58 found that the lumbar facet joints resist approximately 16% of the intervertebral compressive force
when standing erect versus near 0% when sitting,
which helps explain the high intradiscal pressures
during unsupported sitting.59 Finally, after conducting
in vitro experiments measuring induced loads on cadaveric lumbar facets, Lorenz et al.60 concluded that
with increasing compressive loads, the absolute facet
loads increases only slightly, so that the proportion of
the axial burden borne by the l-z joints actually decreases with increasing stress. During extension, the
normal load on the facet joints is always higher when
compared with the neutral mode. After facetectomy,
while the remaining load on the vestigial facet is
substantially reduced, the peak pressure increases.60
In summary, the l-z joints serve primarily a protective
role, functioning to limit movement in all planes of
motion. Whereas they do play a part in weight bearing, the proportion of the axial load they bear is
inversely proportional to the amount of stress.
Mechanisms of Injury
Fig. 3. Segmental variation in lumbar zygapophysial facet joint
orientation in the transverse plane. Adapted from Taylor and
Twomey277 and Masharawi et al.46 Drawings by Specialist Frank
and Angela Dill, US Army, and Frank M. Cort, M.S. (Research
Associate, Department of Radiology, Johns Hopkins Hospital,
Baltimore, Maryland).
of supporting almost twice body weight.23 As aging
occurs, the joints become weaker and more biplanar,
transitioning from a largely coronal orientation to a more
prominent sagittal positioning. The orientation of each
joint to the sagittal plane can also differ between the
paired facet joints at the same spinal level. This phenomenon is known as tropism and has a 20 – 40% incidence
among the general population.24,50 Most50 –55 but not
all49,56 studies have demonstrated a positive relation
between facet joint tropism and intervertebral disc degeneration and herniation.
Although most of the axial load is borne by the
intervertebral discs, the two other components of the
three-joint complex, the l-z joints, also play a role in
weight bearing, with the proportion dependent on
several factors. In a study by Yang and King,57 the
authors determined that normal facet joints typically
carry 3–25% of the axial burden, which can increase
even higher in patients with degenerative disc disease
facet arthritis. During this seminal experiment, it was
observed that with significant facet loading the infeAnesthesiology, V 106, No 3, Mar 2007
Cadaveric and Animal Studies
Although in rare instances the development of facet
joint arthropathy can be traced to a specific inciting
event,61 the overwhelming majority of cases of l-z joint
pain are the result of repetitive strain and/or low-grade
trauma accumulated over the course of a lifetime. Khalsa
et al. conducted a series of cadaveric experiments designed to determine which physiologic movements are
associated with the greatest degree of facet joint capsule
strains. They found that the joint moments measured at
any given motion increased with greater magnitudes of
joint displacement, and were significantly larger in the
two most caudad facet joints (L4 –L5 and L5–S1).62 With
lateral bending, strains of the joint capsule tended to be
larger in magnitude in the three most caudad joints
(L3–S1) during contralateral flexion (i.e., the left facet
joints are most strained during right lateral flexion),
whereas the two most cephalad joints (L1–L2 and L2–L3)
bore the greatest strain during bending to the ipsilateral
side. For the upper three facet joints, the maximum joint
displacement and greatest strain was associated with
lateral bending, usually to the right. For the two lowest
joints, the greatest degree of strain occurred during
forward flexion (table 1).
In a follow-up study, the authors fixated human lumbar
spine specimens with a single anterior thoracolumbar
plate on L4 –L5, and then measured capsular displace-
595
Table 1. Motions Associated with the Largest Intervertebral
Angulation and Strain for the Lumbar Facet Joints
Facet Joint
Level
L1–L2
L2–L3
L3–L4
L4–L5
L5–S1
Movement Associated
with Maximal IVA
Right bending
Left bending
Right bending
Forward flexion
Extension
Largest Strain
Right bending
Right bending
Right bending
Forward flexion
Forward flexion
IVA ⫽ intervertebral angle.
Modified from Ianuzzi et al.62
ment and strains for a wide range of physiologic motions.63 For all motions, increased joint moments occurred at the level of fixation and both adjacent levels.
There was also an increase in intervertebral angulation at
L3–L4 and L5–S1, and decreased motion at L4 –L5. Increased strain was noted bilaterally at L3–L4 and L5–S1,
and contralaterally at L4 –L5. On the side ipsilateral to
the fixation, decreased strain was found at L4 –L5. These
findings support the work of other investigators demonstrating that fusing two vertebrae results in a transfer of
motion previously occurring at the operated level to
adjacent segments, particularly L5–S1, which in turn can
lead to accelerated degeneration.64 – 68
In a subsequent study, Little and Khalsa69 found that
both sustained and repetitive lumbar flexion increased
capsular motion and joint strain from L3–L4 to L5–S1,
with creep developing more rapidly during sustained
flexion than with repetitive movements. Interestingly,
these parameters remained elevated even after a 20-min
recovery period. Although these studies provide a theoretical framework for the development of microinjury
associated with repetitive spine movements, cadavers
cannot experience pain, and the viscoelastic material
properties factored into computational cadaveric spine
models may differ from those found in live patients.70
In response to repetitive strain and inflammation, the
synovial l-z joints can fill with fluid and distend, resulting
in pain from stretching the joint capsule.71 Distension of
the articular recesses can also compress the exiting
nerve root in the neural foramen or spinal canal, especially when the foramen is already narrowed by joint
hypertrophy and/or osteophytes. 72–75 This can lead to
concomitant sciatica and mask the facet pathology underlying the radiculopathy. Capsular irritation may also
result in reflex spasm of the erector spinae, multifidus,
and other paraspinal muscles.72,76,77
In in vivo and in vitro experiments designed to reproduce facet capsular stretch, nerves typically cease firing
shortly after the stimulus is removed.78 – 80 Although
these findings indicate that capsular strain could cause
acute facetogenic pain, they do not explain its persistence. The pathophysiologic basis for persistent lumbar
facet pain was established in a series of elegant experiments conducted by Cavanaugh, Yamashita, Ozaktay, et
al. in New Zealand white rabbits. In these studies, the
application of inflammatory chemicals or algesic mediators such as substance P and phospholipase A2, were
found to result in inflammatory changes consisting of
vasodilation, venous congestion, and the accumulation
of polymorphonuclear leukocytes. Neuronal sensitization occurred in both nociceptive and proprioceptive
nerve endings, being manifested by reduced mechanical
thresholds, increases in multiunit discharge rate and recruitment of previously silent units.81– 84 Persistent nociceptive input invariably leads to peripheral sensitization, and if the underlying stimulus is not removed,
central sensitization and neuroplasticity can develop.85
Whereas the spinal structures in humans are subject to
greater stress than other mammals, because of the array
of anatomical and functional differences that exist between the l-z joints in various mammalian species,86
caution should be exercised when extrapolating the
results of animal studies to humans.
One inferential interpretation of these preclinical findings is that chronic l-z joint pain is likely to occur with
repetitive, chronic strains as might be seen in the elderly
or, less frequently, after an acute event such as tearing
the joint capsule by stretching it beyond its physiologic
limits. This hypothesis is supported by clinical studies
indicating a higher prevalence of facet arthropathy in
elderly patients87– 89 and numerous cases of lumbar facet
arthropathy after high-energy trauma.61
Human Studies
Clinically, several conditions may predispose individuals to chronic facet joint strain. Radiologic studies conducted in LBP patients and asymptomatic controls have
shown a positive correlation between sagittally oriented
facet joints and degenerative spondylolisthesis.48,49 In
these patients, recurrent rotational strains result in myriad changes to the discs and paired l-z joints, including
loss of disc height, osteophyte formation, and degenerative hypertrophy of the facets.90,91
Changes in any component of the three-joint spinal
unit lead to predictable changes in the other components. Degeneration and loss of structural integrity of
the intervertebral discs have been shown to result in
concomitant degenerative changes in the l-z
joints.92–94 The reverse is also true. Degeneration and
motion abnormalities at the l-z joints can induce and
accelerate degeneration of the intervertebral
discs.58,95,96 In a magnetic resonance imaging (MRI)
study evaluating the relation between facet joint osteoarthritis and degenerative disc disease (DDD), Fujiwara et al. 97 found that facet joint osteoarthritis was
rarely found in the absence of disc degeneration but
tended to be most pronounced at spinal levels associated with advanced DDD. The authors concluded that
disc degeneration is a more reliable indicator of aging
596
than facet joint osteoarthritis, and in most people,
DDD precedes facet osteoarthritis.
Paradoxically, in the only clinical study evaluating the
relative contributions of DDD and facet arthropathy to
chronic LBP, Schwarzer et al.98 found the combination
of discogenic and l-z joint pain to be a relatively rare
occurrence. In 92 patients who underwent both discography and confirmatory l-z joint blocks with lidocaine
and bupivacaine, 39% had at least one positive discogram with a negative control disc, and 9% obtained
concordant pain relief after the series of analgesic facet
joint blocks. But only 3% of patients had both positive
discography and a symptomatic l-z joint. The discrepancy between the handful of basic science studies demonstrating a correlation between DDD and facet joint
degeneration and the lone clinical study finding minimal
overlap between the two pain generators indicates that
more research is needed on this topic.
Aside from osteoarthritis, several other conditions may
affect the facet joints. These include inflammatory arthritides such as rheumatoid arthritis, ankylosing spondylitis and reactive arthritis,99 –101 synovial impingement,
meniscoid entrapment, chondromalacia facetae, pseudogout, synovial inflammation, villonodular synovitis, and
acute and chronic infection.102–106 Intrafacetal synovial
cysts can be a source of pain because of distension and
pressure on adjacent pain-generating structures, calcification, and asymmetrical facet hypertrophy.107–110 In a
retrospective review of MRI scans in 303 consecutive
patients with LBP, Doyle and Merrilees111 found that
9.5% had facet joint synovial cysts, the large majority of
which were located posteriorly. Trauma may also cause
lumbar facetogenic pain. There are more than two dozen
reported cases of lumbar facet dislocation after rapid
deceleration injuries (e.g., traffic accidents), most involving L5–S1.61,112–115 The mechanism of injury in these
cases is purported to be a combination of hyperflexion,
distraction, and rotation.61,112,116 In a posthumous study
conducted in 31 lumbar spines of subjects who died of
traumatic injuries (mostly motor vehicle accidents),
Twomey et al.117 found occult bony fractures in the
superior articular process or subchondral bone plate in
35% of victims, and z-joint capsular and/or articularcartilage damage in 77% of cases. The authors concluded
that occult bony and soft tissue injuries to the l-z joints
may be a common cause of LBP after trauma.
Prevalence
The prevalence rate of l-z joint pain varies widely in
the literature, ranging from less than 5% to upward of
90%.118 –125 To a large extent, the wide discrepancy in
prevalence rates is a function of the diagnostic methodology used and the perspective and conviction of
the investigator. Numerous reviews have outlined the
inherent flaws in diagnosing l-z joint pain using historic, physical examination, and radiologic findings
and concluded that an analgesic response to imageguided intraarticular or MBB is the only reliable and
valid method to identify a facet joint(s) as the primary
pain generator.126 –128 Furthermore, the false-positive
rate of uncontrolled facet blocks has been found to
range between 25% and 41% using comparative LA
injections or saline controls,129 –132 leading some experts to conclude that the use of controlled blocks is
the only reliable means to diagnose lumbar facetogenic pain.133
Using single LA blocks, the prevalence of l-z joint pain
has been reported to range from 8% to 94%.89,119 When
placebo-controlled and comparative LA facet blocks are
used, the reported prevalence rates decline significantly,
ranging from 9% to 42%.98,131 The estimated prevalence
rates increase in conjunction with age in the populations
studied. In a comprehensive epidemiologic study on
LBP, spine surgeons from eight academic medical centers in the United States collected demographic and
clinical information on more than 4,000 patients during
a 5-yr period.118 Final diagnoses were rendered based on
historic and physical examination findings, radiologic
and other diagnostic studies, and response to treatment
and/or diagnostic injections. Among the 2,374 patients
who remained in the study, “facet joint arthritis” was the
final diagnosis in 4.8% of cases. In an epidemiologic
study conducted in a primary care setting, l-z joint pain
was estimated to account for approximately 6% of patients with chronic LBP.134 Based on studies using comparative or controlled blocks, in descending order, the
L5–S1, L4 –L5, and L3–L4 facet joints are most frequently
implicated in l-z joint pain.98,130,132
One problem that emerges when synthesizing data
from published prevalence studies is that almost all
excluded patients with neurologic signs or symptoms
secondary to a herniated disc, the most common cause
of chronic LBP, and many excluded patients with
previous back surgery. In patients with facet hypertrophy, foraminal narrowing can actually cause radicular symptoms.72–74,135 A second confounding factor
is that the best prevalence studies used comparative
MBB to estimate l-z joint pain. The primary dorsal rami
divide into three nerves as they approach their respective transverse processes, the largest of which is the
medial branch. In addition to supplying two facet
joints, the medial branch also innervates the multifidus, interspinales muscle and ligament, and the periosteum of the neural arch. The two other main
branches of the dorsal ramus are the intermediate
branch, which sends fibers into the longissimus muscle, and the lateral branch, which innervates the iliocostalis muscle, the thoracolumbar fascia, the skin of
the lower back and buttock, and the sacroiliac
joint.29,136,137 At the superomedial border of the trans-
verse processes where the lumbar medial branches are
most amenable to blockade, these nerves are in such
close proximity that anesthetizing any one of them
will almost invariably lead to blockade of the others
branches of the primary dorsal rami. Therefore, MBB
may not only block nociceptive signals arising from
the l-z joints, but also from several other potential
pain-generating structures around the lumbar spine.
This makes the true prevalence rate of l-z joint pain
exceedingly difficult to estimate. Based on the evidence that does exist, the lumbar facet joints seem to
be the primary pain generator in approximately 10 –
15% of chronic LBP patients (table 2).
Pain Referral Patterns
In an attempt to better understand l-z joint pain, many
investigators have attempted to identify pain referral
patterns using a variety of different methods. These include pain provocation via stimulation of the facet joint
capsules and medial branches in pain patients and
asymptomatic volunteers, and mapping out pain diagrams in subjects in whom pain was relieved by the
injection of LA, with or without steroid. For the most
part, these studies have not demonstrated any reliable
pain referral pattern stemming from any of the l-z joints.
Discrepancies between pain provocation and pain patterns/histologic findings have been found not only for l-z
joint stimulation,138,139 but also during sacroiliac joint
and selective nerve root blocks.140,141 Part of the problem with using provocative tests to delineate pain referral patterns is that artificial stimulation of the l-z joints
and/or their nerve supply may not simulate physiologic
conditions.
Nevertheless, certain patterns do emerge when synthesizing the existing data. To summarize these findings, the
joint capsule seems to be more likely to generate pain
than the synovium or articular cartilage. There is also
considerable overlap between all lumbar facet joints,
with the referral pattern being more widespread and
variable in patients with chronic pain than in asymptomatic volunteers. All of the lumbar facet joints are capable
of producing pain that can be referred into the groin,
although this is more common with lower facet joint
pathology. Pain emanating from upper facet joints tends
to extend into the flank, hip, and upper lateral thigh,
whereas pain from the lower facet joints is likely to
penetrate deeper into the thigh, usually laterally and/or
posteriorly. Infrequently, the L4 –L5 and L5–S1 facet
joints can provoke pain extending into the lower lateral
leg and, in rare instances, even the foot. In patients with
osteophytes, synovial cysts, or facet hypertrophy, the
presence of radicular symptoms may also accompany
sclerotomal referral patterns (table 3 and fig. 4).
597
Diagnosis
History and Physical Examination
Numerous studies have attempted to delineate a discrete set of historic and physical findings pathognomonic or at least suggestive of lumbar facet arthropathy.
Fairbank et al.142 conducted a prospective study in 41
patients with acute LBP whereby two-level intraarticular
facet blocks were performed with low-volume bupivacaine. Among the 25 patients who completed the study,
14 obtained at least temporary relief after the injections.
Compared with nonresponders, responders tended to
have pain localized to the back and thigh, and to report
pain during forward flexion.
In 1988, Helbig and Lee143 designated a “lumbar facet
syndrome” based on a retrospective study conducted in
22 patients. The authors found that patients who responded to intraarticular facet injections (injection parameters not noted) were more likely to have back pain
associated with groin or thigh pain, paraspinal tenderness, and reproduction of pain during extension–rotation maneuvers. Pain radiating below the knee was negatively associated with a positive response to facet
blocks.
Despite the widespread acceptance of the “lumbar
facet syndrome,” a multitude of larger and more methodologically sound studies have failed to duplicate the
findings of Helbig and Lee. In a large study conducted in
390 patients with chronic LBP, Jackson et al.89 were
unable to identify any historic or physical examination
variables associated with analgesic response to facet
injections. Schwarzer et al.12 conducted a prospective
study attempting to identify clinical features in 176 patients with chronic LBP undergoing double, confirmatory blocks. In the 15% of patients who achieved concordant pain relief with lidocaine and bupivacaine, no
clinical feature was associated with a positive response.
In a randomized, placebo-controlled study performed on
80 patients with chronic LBP, Revel et al.88 identified
seven variables associated with a positive response to
facet joint anesthesia: age greater than 65 yr and pain not
exacerbated by coughing, not worsened by hyperextension, not worsened by forward flexion, not worsened
when rising from forward flexion, not worsened by
extension–rotation, and well-relieved by recumbency.
However, subsequent investigations have also failed to
corroborate the findings of Revel et al. (table 4). In
summary, no historic or physical examination findings
can reliably predict response to diagnostic facet joint
blocks.
Radiologic Findings
The prevalence of abnormal l-z joint changes on radiologic imaging depends on the age and presence of symptoms in the study population, the imaging modality used,
and the threshold use for rendering a diagnosis of “ab-
598
Table 2. Results of Lumbar Zygapophysial Joint Pain Prevalence Studies Conducted Using Either Placebo-controlled or
Comparative Local Anesthetic Blocks
Author, Year
Patients
Interventions
Results
False-positive Rate and
Comments
Schwarzer et al.,98 1994
92 pts with chronic LBP
without neurologic
deficit or previous
surgery. All pts
underwent
comparative facet
blocks and
provocative
discography.
without neurologic
deficit or previous
surgery.
Pts rec’d either intraarticular
(0.5 ml) or MBB (0.5 ml)
with 2% lidocaine at 3
lowest facet levels. In pts
who obtained ⱖ 50% relief,
blocks were repeated with
0.5% bupivacaine. A (⫹)
response was pain relief
sustained for ⱖ 3 h.
Pts rec’d either intraarticular or
MBB (0.5 ml) with 2%
lidocaine at 3 lowest levels.
In pts who obtained ⱖ 50%
pain relief, blocks were
repeated with 0.5%
bupivacaine. A (⫹) response
was pain relief sustained for
ⱖ 3 h.
Pts rec’d placebo injections
followed by single-level
intraarticular facet injections
(up to 1.5 ml bupivacaine,
0.5%) at 3 lowest levels, on
separate occasions. A (⫹)
response was pain relief
sustained for ⱖ 3 h only
with bupivacaine.
Pts rec’d either placebo or 1
ml lidocaine injected into
the 2 most caudad facet
joints. A (⫹) response
was ⬎ 75% pain relief.
Pts rec’d MBB with 0.4–0.6 ml
of 1% lidocaine and/or
0.25% bupivacaine. A (⫹)
response was ⱖ 75% relief
lasting longer with
bupivacaine than lidocaine.
39% of pts (n ⫽ 36) achieved
definite pain relief after
lidocaine blocks. 25% of pts
who underwent confirmatory
blocks with bupivacaine
obtained had a (⫹)
response, for a 9%
prevalence rate.
26% rate of FP blocks. 39% of
pts had (⫹) discography.
Only 3 pts had both (⫹)
discography and (⫹)
response to facet blocks.
Median age 37 yr.
Male:female ratio was 2:1.
47% of pts (n ⫽ 83) reported a
definite or greater response
after lidocaine, with 26 of 71
pts who underwent
confirmatory blocks
obtaining concordant relief,
for a prevalence rate of
15%.
FP rate of 38%. Median age 38
yr.
40% obtained ⬎ 50% pain
relief with bupivacaine but
not placebo. 37%
had ⬎ 90% pain relief.
32% of pts obtained ⬎ 50%
pain relief for ⱖ 3 h after
placebo. 18 of 23 obtained
relief at only 1 level. Median
age 59 yr. Female:male ratio
was 3:1.
31% of lidocaine group
obtained significant pain
relief after the injection.
18% of pts receiving
intraarticular saline obtained
significant pain relief. Mean
age 58 yr. 2:1 female:male
ratio.
FP rate was 41%. Pts who had
previous surgery were less
likely to have l-z joint pain.
Trauma was implicated as
cause of pain in 53% of pts.
Mean age 47 yr.
without neurologic
deficit or previous
surgery.
Revel et al.,88 1998
not due to sciatica,
without previous
surgery.
Manchikanti et al.,131
1999
without neurologic
deficit.
2000
without neurologic
deficits.
Dreyfuss et al.,182 2000
41 carefully chosen pts
out of 138 screened
by telephone interview
with chronic LBP, no
neurologic deficits,
and an absence of
psychiatric or severe
concomitant spinal
pathology.
without neurologic
deficits.
2000
2004
without neurologic
deficits.
Pts rec’d double MBB from
L1–L5 with 0.5 ml lidocaine
and bupivacaine, LA with
Sarapin (High Chemical,
Levitown, PA), or LA with
Sarapin and steroid. A (⫹)
response was ⱖ 75% relief
lasting longer with
bupivacaine than lidocaine.
Pts rec’d MBB with 2%
lidocaine at maximally
tender areas. Pts who
obtained ⱖ 80% pain relief
underwent confirmatory
blocks with bupivacaine. A
(⫹) response was definite
pain relief lasting ⬎ 2 h.
lidocaine. All pts who
blocks with 0.25%
was ⱖ 75% relief lasting
longer with bupivacaine.
lidocaine. All pts who
blocks with 0.25%
was ⱖ 80% relief lasting
longer with bupivacaine.
81 pts (67.5%) reported a
definite response to
lidocaine MBB. 54 of these
reported definite pain relief
after the bupivacaine block,
for a prevalence rate of
45%.
74% of pts (n ⫽ 133) obtained
a (⫹) response to the
lidocaine blocks, but only 65
reported definite pain relief
after bupivacaine blocks, for
a 36% prevalence rate.
25% FP rate. Mean age was 48
yr.
22 pts obtained significant
pain relief after lidocaine
MBB, with 15
obtaining ⱖ 80% after
bupivacaine blocks, for a
37% prevalence rate.
FP rate of 17%. Mean age 55
yr in 15 responders. Pts
carefully chosen to evaluate
outcomes for radiofrequency
denervation.
64% (n ⫽ 127) reported a (⫹)
response to lidocaine
blocks, with 84 obtaining
definite pain relief after
bupivacaine blocks, for a
42% prevalence rate.
37% FP rate. Mean age 47 yr.
198 (50%) of pts obtained a
(⫹) response to lidocaine
blocks, with 124 reporting
definite pain relief with
bupivacaine, for a 31%
prevalence rate.
FP rate was 27%. Mean age 47
yr.
False-positive (FP) rate: If not mentioned, this was determined by dividing the number of patients who obtained pain relief with the lidocaine screening block but
not by the confirmatory block by the total number of blocks.
LA ⫽ local anesthetic; LBP ⫽ low back pain; MBB ⫽ medial branch block; pts ⫽ patients; rec’d ⫽ received.
normal” (table 5). In studies conducted in patients with
LBP, the incidence of degenerative facet disease on computed tomographic (CT) scanning ranges from around
40% in some studies125,144 to upwards of 85% in othAnesthesiology, V 106, No 3, Mar 2007
ers.119 MRI is considered to be somewhat less sensitive
than CT imaging for detecting degenerative facet changes,119,145,146 although several studies conducted in
chronic LBP patients found both the sensitivity and spec-
599
Table 3. Results of Studies Examining PAIN referral Patterns for Lumbar Zygapophysial Joint Pain
Author, Year
7
Hirsch et al., 1963
Mooney and Robertson,9 1976
Patients and Interventions
Number of pts and characteristics not mentioned.
Injected ⬍ 0.3 ml hypertonic NS, 11%, into one
of the lower facet joints.
5 controls and 15 pts with chronic LBP. Injected
1–3 ml hypertonic NS, 5%, into L3–L4 through
L5–S1 facet joints, and S1–S2 in pts with
lumbarization of the sacrum.
McCall et al.,10 1979
Injected 0.4 ml hypertonic saline, 6%,
intracapsular and pericapsular, into the L1–L2
and L4–L5 facet joints of 6 asymptomatic male
volunteers.
Fairbank et al.,142 1981
25 pts with acute back and/or leg pain underwent
l-z joint injections at the area of maximal
tenderness and 1 additional randomly chosen
joint with 0.5 ml bupivacaine.
Retrospective review of 99 pts with LBP of varying
duration who underwent l-z joint injections with
1 ml lidocaine and steroid.
50 pts with chronic LBP diagnosed by physical
examination and x-rays as having facet pain
underwent intraarticular steroid injections in 1 or
2 lower facet joints.
Lippitt,205 1984
Lynch and Taylor,268 1986
Helbig and Lee,143 1988
Jackson et al.,89 1988
Marks et al.,269 1989
Kuslich et al.,11 1991
Marks,8 1992
Retrospective review of 22 pts with chronic low
back and leg pain. Injected l-z joint(s) with LA
and steroid. Divided pts into (⫺) response (no
relief), temporary response (relief lasted ⬎ a few
h but ⬍ 6 mo), and prolonged response (⬎ 6 mo
relief).
390 pts with low back and no neurologic signs
underwent L4–L5 and L5–S1 l-z joint injections
with steroid and 1 ml bupivacaine.
138 pts with chronic LBP underwent lumbar facet
and MBB at the same levels. Blocks performed
with 1.0 ml lidocaine, except at L5–S1, where
1.5 ml was used.
193 pts undergoing decompression surgery during
local anesthesia. Stimulated a variety of tissue,
included l-z joints by mechanical force or
unipolar cautery.
86 pts with chronic LBP receive either l-z joint or
MBB with steroid and 1 or 1.5 (at L5–S1 or the
L5 dorsal ramus) ml LA.
90 pts with chronic LBP underwent l-z joint blocks
with 0.8 ml contrast and lidocaine at 3 levels.
Fukui et al.,270 1997
48 pts with chronic LBP underwent l-z joint blocks
with contrast until pain was provoked, then rec’d
0.5–1 ml LA. Pts who obtained excellent but
temporary relief proceeded to RF denervation,
with electrical stimulation used to locate the
target nerve.
Kaplan et al.,32 1998
15 asymptomatic pts underwent painful facet
capsular distension with up to 2.5 ml contrast.
Manchikanti et al.,131 1999
120 pts with chronic LBP and no neurologic
deficits underwent confirmatory MBB with 0.4–
0.6 ml lidocaine and bupivacaine.
200 pts with chronic LBP without neurologic
deficits underwent confirmatory MBB with 0.4–
0.6 ml lidocaine and bupivacaine.
23 pts with chronic LBP and no neurologic deficits
underwent l-z joint injections with ⬍ 1.5 ml LA. A
(⫹) response was designated as both
concordant pain provocation and relief with LA.
Manchikanti et al.,266 2000
Young et al.,271 2003
Results
Pain distributed to SI joint and gluteal areas, then out
to greater trochanter. Pain identical to typical LBP.
L3–L4 produced pain radiating down lateral aspect of
leg. L4–L5 and L5–S1 produced pain radiating
posteriorly down the leg, often below the knee in pts
with LBP. If present, S1–S2 produced pain radiating
under buttock. Increasing volume increased amount
of radiation. Pts with LBP had greater radiation than
pts without back pain.
There was little difference in pain distribution between
intracapsular and pericapsular injections. Pain from
L4–L5 radiated to the flank, buttock, iliac crest,
upper and lower groin, and thigh above the knee.
Pain from L1–L2 radiated to the flank, iliac crest,
upper groin, and occasionally the abdomen. Pain
never radiated contralaterally.
Responders had pain in the back and thigh, whereas
nonresponders had pain in back and lower leg.
Symptomatic pain reproduction occurred only in 6
pts.
No pattern of pain was noted to be more common in
responders. Included pts with unilateral or bilateral
hip pain, buttock pain, or pain localized to low back.
39 pts reported total (n ⫽ 11) or partial (n ⫽ 28) relief
of pain after 2 wk. More than 90% of pts reported
LBP during injection, with half reporting pain
radiating into ipsilateral thigh and buttock. No pt
reported pain below knee.
80% of pts with groin or thigh pain had a prolonged
response. No pt with groin pain and only 1 with thigh
pain had (⫺) response. Pts with pain below knee had
37% (⫺) responses and only 25% prolonged
responses.
Postinjection pain relief was more likely to occur in
patients without leg pain.
The pain produced at all levels was mostly local. The
L4–L5 and L5–S1 joints were also likely to radiate to
buttock, greater trochanter, and all aspects of thigh.
Approximately 5% of time, pain extended below
knee. Pain from L2–L5 sometimes extended to groin.
Stimulation of nerves was more likely to produce
distally referred pain than intraarticular provocation.
Facet capsule stimulation produced pain in 30% of pts,
but “significant pain” only 2.5% of time. Pain
radiated into back and buttock, but never the leg.
No pattern of pain predicted response to injection. Pts
were included who had axial pain and pain radiating
to the leg.
Based on analgesic response to a single block, there
was a significant association between concordant
pain provocation and pain relief. However, based on
concordant analgesic response to serial lidocaine
and bupivacaine blocks, there was no association
between pain provocation and pain relief.
Intraarticular contrast injection always reproduced a
pt’s pain. Pain from L1–L2 joint always produced
lumbar pain. In descending order, L2–L3 joint
produced pain in the lumbar region, hip, and buttock
or lateral thigh. L3–L4 produced pain mostly in the
lumbar region, buttock, or lateral/posterior thigh. L4–
L5 elicited pain in the lumbar region, buttock, or
lateral thigh. L5–S1 elicited pain in the lumbar region,
buttock, lateral thigh, or posterior thigh. Pain relief
from stimulation of medial branches was similar to
that of l-z joints.
All subjects experienced a well-circumscribed area of
pain without radiation into the inferior buttock or
extremity.
were included who had axial pain only, thigh pain,
groin pain, and leg pain.
were included who had axial pain only, thigh pain,
groin pain, and/or leg pain.
The location of pain (radiating toward or away from the
spinal column) was not associated with a (⫹)
response.
LA ⫽ local anesthetic; LBP ⫽ low back pain; l-z ⫽ lumbar zygapophysial; MBB ⫽ medial branch block; NS ⫽ normal saline; pts ⫽ patients; rec’d ⫽ received;
RF ⫽ radiofrequency; SI ⫽ sacroiliac.
600
Fig. 4. Pain referral patterns from the lumbar facet joints. In
descending order, the most common referral patterns extend
from the darkest (low back) to the lightest regions (flank and
foot). The key at the bottom of the figure legend is listed in
order of affected frequency (i.e., low back to foot). The facet
levels next to each location represent the zygapophysial joints
associated with pain in each region. Data adapted from McCall
et al.,10 Marks,269 and Fukui et al.270 Drawings by Specialist
Frank and Angela Dill, US Army, and Frank M. Cort, M.S. (Research Associate, Department of Radiology, Johns Hopkins Hospital, Baltimore, Maryland). Low back: L5–S1, L4 –L5, L3–L4 Buttock: L5–S1, L4 –L5, L3–L4 Lateral thigh: L5–S1, L4 –L5, L3–L4,
L2–L3 Posterior thigh: L5–S1, L4 –L5, L3–L4 Greater trochanter:
L5–S1, L4 –L5, L3–L4, L2–L3 Groin: L5–S1, L4 –L5, L3–L4, L2–L3,
L1–L2 Anterior thigh: L5–S1, L4 –L5, L3–L4 Lateral lower leg:
L5–S1, L4 –L5, L3–L4 Upper back: L3–L4, L2–L3, L1–L2 Flank:
L1–L2, L2–L3 Foot: L5–S1, L4 –L5
ificity of MRI to be more than 90% compared with
CT.97,145 In a study by Fujiwara et al.97 conducted in 14
subjects with DDD, the extent of lumbar facet osteoarthritic changes was minimal in patients younger than 40
yr. In patients older than 60 yr, the prevalence of degenerative changes increased significantly but was by no
means universal. No facet osteoarthritis was observed in
any patient in the absence of disc degeneration. In CT
and MRI studies conducted in asymptomatic volunteers,
the prevalence of facet degeneration ranges from 8% to
14%.147–149 In one study by Weishaupt et al.147 conducted in 60 asymptomatic volunteers aged 20 –50 yr,
disc bulging or protrusion was found in 37 and 40
subjects, but severe osteoarthritis of the facet joints was
absent in all 60 subjects. The authors suggested that
severe osteoarthritis of the l-z joints may play a prominent role in LBP because of its absence in asymptomatic
individuals.
The ability of radiologic imaging to predict response to
diagnostic l-z joint blocks has been conflicting at best.
Whereas some studies have found a positive correlation
between CT, MRI, or other imaging studies and response
to l-z joint blocks,124,125,143,144,150 an equal number have
not.87,89,119,142,151,152 Results from the three largest studies have also been mixed. The largest study, by Jackson
et al.,89 found no relation between radiographic evidence of l-z joint degeneration and response to single,
intraarticular facet injections in 390 patients. This is in
contrast to Carrera and Williams,144 who found that 73%
of chronic LBP patients (n ⫽ 63) demonstrating CT
evidence of lumbar facet disease experienced pain relief
after large-volume (2– 4 ml) facet blocks versus only 13%
in whom CT scans showed no pathology. In the only
study using placebo-controlled blocks to confirm a diagnosis of l-z joint pain, Schwarzer et al.152 found no
correlation between CT findings and a positive response
to LA but not saline blocks in 63 patients. The results of
Jackson et al. and Schwarzer et al. support clinical studies showing no correlation between MRI findings and
results of medial branch radiofrequency denervation. In
a study by Cohen et al.153 conducted in 192 patients
who underwent radiofrequency denervation based on a
positive response to single MBB, the authors found no
association between MRI evidence of facet hypertrophy
or degeneration and 6-month outcomes. Finally,
Kawaguchi et al.154 found no significant association between the degree of radiographic lumbar facet joint
abnormalities and LBP symptoms in a study conducted in
106 patients with rheumatoid arthritis. In summary, the
evidence in the literature does not support the routine
use of radiologic imaging to diagnose l-z joint pain.
Diagnostic Blocks
It is generally accepted in clinical practice that diagnostic blocks are the most reliable means for diagnosing
l-z joints as pain generators. Numerous guidelines and
reviews have asserted that intraarticular injections and
MBB are equally effective in diagnosing l-z joint
pain.105,126,127,133 Although this statement may seem to
have face validity, several factors may undermine the
utility of diagnostic blocks, especially MBB. In a cadaveric study, Kellegren155 showed that 0.5 ml injectate
spread into an area encompassing 6 cm2 of tissue. In
view of the close proximity of the medial branch nerves
to the lateral and intermediate branches, even the injection of a low-volume of anesthetic is likely to block these
nerves. Because these nerves, along with the medial
branches themselves, contribute heavily to the innervation of the paraspinal muscles and fascia, ligaments,
sacroiliac joints, and skin, MBB can relieve LBP even in
the presence of normal l-z joints.
Whereas properly performed intraarticular facet injections may be inherently more accurate in diagnosing l-z
joint pain, these blocks can be technically challenging
and fraught with their own limitations. After injecting
somewhere between 1 and 2 ml of fluid, the joint capsule is likely to rupture, with the excess injectate extrav-
601
Table 4. Studies Evaluating the Ability of Historic and Physical Examination Findings to Predict Response to Diagnostic Lumbar
Facet Injections
Author, Year
Results
Comments
Fairbank et al.,142 1981
25 pts with acute LBP rec’d
intraarticular facet injections at 2
levels with 0.5 ml LA.
Helbig and Lee,143 1988
Retrospective study conducted in
22 pts with LBP and leg pain.
Injection parameters not noted.
8 pts obtained relief lasting 1–48 h,
and 6 obtained long-term relief. No
difference between groups in
duration of sx, disability scores, or
psychological profile.
23% of pts had a negative response,
27% had a temporary response,
and 50% a prolonged response.
Lewinnek and
Warfield,124 1986
Retrospective study conducted in
21 pts. Intraarticular injections
performed with LA and steroid.
Jackson et al.,89 1988
390 pts with LBP underwent
intraarticular LA and steroid
injections at L4–L5 and L5–S1
with 1.5 ml.
Lilius et al.,272 1990
109 pts with unilateral chronic LBP
were randomly assigned to
receive either 8 ml LA and
steroid into 2 facet joints, around
2 facet joints, or NS into 2 facet
joints.
40 pts with chronic LBP underwent
intraarticular facet injections with
1.5 ml LA.
Responders had pain localized to back
and thigh, whereas nonresponders
had pain in lower leg. Responders
tended to report more pain during
forward flexion.
Back pain radiating to groin or thigh,
paraspinal tenderness, and
reproduction of pain with extension–
rotation associated with (⫹) response.
Pain extending below knee associated
with (⫺) response.
Negative screening examination for other
causes of LBP or sciatica and
paraspinal tenderness over one or
more facet joints associated with (⫹)
response.
Unable to identify a “facet syndrome.”
Factors associated with a (⫹)
response were older age, absence of
leg pain, and absence of pain with
Valsalva.
No clinical finding was associated with
outcome. The number of
“inappropriate signs or sx” and
previous back surgery were positively
associated with failure.
Schwarzer et al.,130
1994
Schwarzer et al.,132
1995
1999
2000
2000
Young et al.,271 2003
Laslett et al.,273 2004
Laslett et al.,274 2006
underwent confirmatory medial
branch or facet blocks with 0.5
ml LA.
LA and NS.
1 ml LA or NS.
underwent confirmatory MBB
with 0.4–0.6 ml LA.
with 0.4–0.6 ml LA mixed with or
without Sarapin (High Chemical,
Levitown, PA) and steroid.
with 0.4–0.6 ml LA.
⬍ 1.5 ml LA.
111 pts underwent intraarticular or
MBB with 0.5 ml LA. Study
designed to confirm Revel’s
findings.88
151 pts underwent confirmatory
MBB or intraarticular injections
with 0.5 ml LA.
75% of pts had an initial (⫹)
response, but only 33% had a
response lasting ⬎ 3 mo.
7.7% reported complete pain relief
after injection.
Approximately 30% of pts showed
significant improvement. Pain relief
at 1 h after injection correlated
with pain relief at 3 mo after
injection. No basis for large
volumes injected.
55% had (⫹) response to injection,
of which 43% had ⬎ 90% relief.
Factors associated with a (⫹) response
were older age, absence of pain
exacerbation by coughing, relief when
recumbent, absence of exacerbation
by forward flexion and rising from
forward flexion, absence of
exacerbation by hyperextension, and
absence of exacerbation by
extension–rotation.
No statistically significant association
between response to blocks found for
any feature on history or PE.
15% responded with concordant
relief to lidocaine and confirmatory
bupivacaine blocks.
No historic PE finding could distinguish
pts with (⫹) response to blocks.
40% of pts obtained significant relief
with LA but not NS.
Factors associated with a (⫹) response
were older age, absence of pain
exacerbation by coughing, relief when
recumbent, absence of exacerbation
by forward flexion and rising from
forward flexion, absence of
exacerbation by hyperextension, and
absence of exacerbation by
extension–rotation.
Only historic or PE finding associated
with a (⫹) response was absence of
back pain with straight leg raising.
Only historic or PE finding associated
with a (⫹) response was absence of
back or leg pain with straight leg
raising.
Results identical to previous
uncontrolled study. Presence of 5
of 7 variables distinguished 92%
of responders and 80% of
nonresponders.
Only clinical feature associated with (⫹)
response was relief of pain in supine
position. Negative correlation between
exacerbation of back pain with straight
leg raising and (⫹) block.
Only lack of pain provocation when
rising from sitting was associated with
(⫹) response.
Only absence of pain with coughing and
absence of pain exacerbation when
rising from flexion showed a trend
toward being associated with a (⫹)
response (P ⫽ 0.07).
Factors associated with (⫹) response
were age ⬎ 50 yr, pain relieved by
walking, pain relieved by sitting, onset
of pain was paraspinal, high
somatization score, pain worsened by
extension–rotation, and absence of
“centralization” of pain.
45% of pts had a concordant (⫹)
response to lidocaine and
bupivacaine blocks.
36% had a concordant (⫹) response
to both blocks.
42% prevalence rate. Negative
correlation between previous
surgery and positive response to
blocks.
61% of pts experienced concordant
pain during injection and relief
after LA instillation.
23% of pts obtained ⱖ 75% pain
relief after block. Pts older than 65
yr were more likely to obtain
complete pain relief.
31 pts excluded. Data missing in
many pts. Utility of predictive
factors diminished with decreasing
pain reduction standards.
LA ⫽ local anesthetic; LBP ⫽ low back pain; MBB ⫽ medial branch block; NS ⫽ normal saline; PE ⫽ physical examination; pts ⫽ patients; rec’d ⫽ received;
sx ⫽ symptoms.
602
Table 5. Levels of Degeneration of Facet Joints based on
Magnetic Resonance Imaging
Grade
Radiologic Findings
0
1
Normal z-joints (2–4 mm width)
Joint space narrowing and/or mild osteophyte formation
and/or mild hypertrophy of the articular process
Narrowing of the joint space with sclerosis or moderate
osteophyte formation and/or moderate hypertrophy of
the articular process and/or mild subarticular bone
erosions
Narrowing of the joint space with marked osteophyte
formation and/or severe hypertrophy of the articular
process and/or severe subarticular bone erosions and/
or subchondral cysts
2
3
Adapted from Weishaupt et al.145; used with permission.
asating into several possible pain-generating structures.
Depending on the point of rupture, these structures may
include the epidural space, intervertebral foramen, ligamentum flavum, and paraspinal musculature.8,71,122,123
There are no crossover studies comparing the validity
of MBB to intraarticular l-z joint injections, and only two
studies comparing them at all. Nash156 conducted a
prospective study in 67 patients with axial LBP who
were randomly assigned in pairs to receive either MBB
with 2 ml LA or intraarticular injections with 1.5 ml LA
and steroid. In the 26 pairs who completed the study, 12
reported MBB to be more beneficial at their 1-month
follow-up, 11 reported the intraarticular injection to be
better, and 3 reported no difference between the two. In
the second study, Marks et al.8 randomly assigned 86
axial LBP patients to receive either intraarticular injections or MBB using 2 ml LA and steroid. The authors
found no difference in the immediate response between
the two groups, although the intraarticular group experienced better pain relief at their 1-month but not
3-month follow-up. There are numerous flaws with these
studies that limit the conclusions one can draw on the
comparative validity of these two procedures, with the
main one being the lack of a definitive diagnosis in the
study subjects. Based on prevalence and false-positive
rates in chronic LBP patients (table 2), MBB and intraarticular seem to provide comparable diagnostic value. In
the four placebo-controlled studies evaluating radiofrequency denervation outcomes in patients with “confirmed” l-z joint pain, the only study that screened patients with MBB demonstrated positive outcomes,157
versus only one of three that used diagnostic intraarticular injections.158 –160 Ultrasound-guided medial branch
and intraarticular blocks have also been demonstrated to
provide comparable accuracy to fluoroscopically guided
injections, although they may be less likely to detect
low-volume intravascular uptake and are less accurate in
obese patients.161–164 Because MBB are technically easier to perform than intraarticular injections and involve
anesthetization of the nerves to be lesioned, it seems
more logical to use these blocks as a prognostic tool
before radiofrequency denervation.
False-positive Blocks
Numerous studies have documented a high false-positive rate for lumbar facet blocks, ranging from 25% to
40% using comparative blocks or saline controls (table
2).128 –130 This rate seems to be unaffected by the type of
block used (i.e., intraarticular or MBB). In a study evaluating the utility of comparative LA MBB versus placebocontrolled MBB to diagnose cervical z-joint, Lord et al.165
found that the use of serial blocks with two different LA
had a high degree of specificity (88%) but only marginal
sensitivity (54%). In addition to the anatomical differences between cervical and lumbar facet joints, this
study used the stringent criterion of “complete or profound pain relief” as the benchmark for a positive block,
leaving the question of extrapolation subject to debate.
However, one interpretation of these findings is that
comparative, LA blocks predispose patients to false-negative diagnoses.
The reasons for false-positive facet blocks are multifactorial and include placebo response (18 –32%) to diagnostic facet interventions, use of sedation, the liberal use
of superficial LA, and the spread of injectate to paingenerating structures other than those targeted.166 Although some investigators have disputed this assertion,167,168 it is our belief that not only opioids, but
sedatives such as midazolam, can lead to false-positive
blocks by interfering with the interpretation of analgesic
response (i.e., preventing a patient from engaging in
normal activities) and virtue of their muscle relaxant
properties.169 In a recent survey conducted in 500 patients receiving facet blocks or epidurals at an outpatient
spine center, only 17% requested sedation.170
Even in patients with symptomatology concordant
with unambiguous pathology, diagnostic blocks may
lack specificity. North et al.171 conducted a prospective
study in 33 patients with L5 or S1 radiculopathy and
radiologic evidence of ongoing nerve root compression.
All patients underwent a battery of LA blocks that included selective nerve root block, sciatic nerve block,
MBB, and subcutaneous control injections. The authors
found that approximately 90% of patients obtained almost complete pain relief after the selective nerve root
block, 70% obtained almost complete relief after the
sciatic block, and a majority received at least 50% pain
relief after the MBB. In contrast, the median degree of
pain relief after the subcutaneous injection was around
30%. The authors concluded that uncontrolled LA blocks
lack specificity in the diagnostic evaluation of referred
pain syndromes.
Dreyfuss et al.31 attempted to measure the specificity
of lumbar MBB by performing 120 fluoroscopically
guided injections in healthy volunteers using 0.5 ml
injectate and identifying the contrast spread using CT
scan. Two target points were chosen, one at the superomedial border of the transverse process and a second
lower site midway between the upper border of the
transverse process and the mamilloaccessory ligament.
Aberrant contrast was noted to spread into the intervertebral foramen or epidural space 16% of the time, being
more common at cephalad spinal levels. When the lower
target points were used, spread into adjacent neural
structures only occurred when a needle was inadvertently placed too high. In all cases, distal spread was
noted into the cleavage plane between the multifidus
and longissimus muscles. In no instance did the 0.5 ml of
contrast fail to bathe the target. The investigators concluded that lower volumes may be adequate for MBB and
that using the lower target point may increase the specificity of lumbar MBB.
Following up on the Dreyfuss study, Cohen et al.135
sought to determine whether spread into the epidural
space or intervertebral foramina could account for falsepositive MBB by examining the relation between clinical
signs of radiculopathy, discographic findings, and radiofrequency outcomes in 78 patients with positive MBB
who went on to fail radiofrequency denervation. The
authors found a negative correlation between discogenic
pain and failed radiofrequency denervation and no association between radicular pain and radiofrequency treatment outcomes. In contrast, there was a trend toward
patients with failed back surgery syndrome to have a
negative outcome after radiofrequency lesioning. The
authors concluded that myofascial pain might be a significant cause of false-positive MBB.
The evidence that the inadvertent treatment of myofascial pain may be a significant cause of false-positive
MBB is circumstantial, but multifaceted. In their large,
multicenter epidemiologic study involving more than
2,000 patients, Long et al.118 found myofascial pain to be
the second most common cause of chronic LBP after
herniated disc. Controlled studies conducted in chronic
LBP patients have shown efficacy for both muscle relaxants and low-volume botulinum toxin injections, and
electromyographic evidence of increased activity compared with matched controls.172–175 Finally, Ackerman
et al.176 tested the hypothesis as to whether myofascial
pain could account for the high rate of false-positive
facet blocks in a double-blind study conducted in 75
men with chronic LBP. Subjects received either intraarticular facet injections or MBB using two techniques:
one in which LA was used to provide superficial anesthesia down to the target point, and a second in which
saline was injected as the needle was advanced. The
authors found that the incidence of postprocedure pain
relief was significantly higher in patients who had LA
injected into their musculature than in those who received saline injected superficially. The injection of LA
into the skin and soft tissues may also reduce LBP by
means other than the inadvertent treatment of myofasAnesthesiology, V 106, No 3, Mar 2007
603
Table 6. Interventions That May Reduce the Incidence of
False-positive Facet Blocks
1. Perform placebo-controlled blocks, or if not possible, comparative local
anesthetic blocks.
2. Aim for a lower target point on the transverse process.
3. Reduce injectate volume to ⬍ 0.5 ml.
4. Be judicious with the use of superficial anesthesia.
5. Consider a single-needle approach.
6. Consider using computed tomographic guidance when doing
intraarticular injections in patients with severe spondylosis.
7. Avoid the use of sedation or intravenous opioids.
cial pain. In studies by Woolf et al.,177,178 the authors
found that the superficial injection of even very small
amounts of lidocaine reduced nociceptive behavior in
animal models of neuropathic pain, a finding attributed
to the systemic absorption of the sodium channel
blocker (table 6).
To reduce the amount of superficial anesthesia used
for MBB, Stojanovic et al.179 introduced the single-needle
technique whereby multiple medial branches are
blocked using a single skin entry point. In a prospective,
crossover study comparing the single-needle and conventional multiple-needle techniques, the authors found
the single-needle technique required significantly less
superficial LA, resulted in less procedure-related pain,
and was quicker to perform than the multiple-needle
approach.180 With regard to final needle position, contrast spread, and postprocedure pain relief, no differences were noted between the two techniques.
False-negative Blocks
False-negative blocks may also occur during diagnostic
facet injections. In a study by Kaplan et al.32 conducted
in 18 asymptomatic volunteers, the authors found that
properly performed MBB result in failure to anesthetize
the corresponding facet joint 11% of the time, even with
the avoidance of venous uptake. Although this may have
occurred because the LA did not engulf the target nerve,
a more likely cause for the false-negative rate is the
presence of aberrant or additional innervation to facet
joints aside from medial branches. In the same study, the
authors found inadvertent venous uptake occurred during 33% of nerve blocks. When the needle was repositioned to avoid venous uptake, analgesia was achieved
only 50% of the time. The authors concluded that when
venous uptake occurs, it may be advantageous to repeat
the procedure on a separate occasion rather than redirecting the needle to avoid false-negative results. In a CT
study by Dreyfuss et al.,31 the authors found inadvertent
venous uptake occurred only 8% of the time.
Should Single or Double Diagnostic Blocks Be Used?
The high rate of false-positive facet blocks has led
numerous experts to advocate performing double
blocks, using either saline controls or two different LA,
before proceeding to definitive therapy.12,128,130 –133,181
604
However, this is rarely done in clinical practice or controlled outcome studies, and there are currently no studies comparing outcomes using single and double blocks.
In the only uncontrolled study assessing outcomes for
medial branch radiofrequency denervation after comparative LA blocks, Dreyfuss et al.182 found that 60% of the
15 patients who proceeded to radiofrequency lesioning
achieved at least 90% pain relief at 12 months, and 87%
achieved at least 60% relief. The basis for undergoing
treatment was at least 80% concordant pain relief after
lidocaine and bupivacaine MBB. However, 460 patients
were interviewed for this study, and after history, physical examination, and record review, only 41 patients
were chosen to participate. Had single blocks or less
stringent criteria been used to designate radiofrequency
candidates, the success rate would have indubitably
been lower in this study, but the total number of successful treatments would have almost certainly been
higher.
When considering whether to perform double
blocks, several factors must be considered, including
the patient’s relative risk for a false-positive block, the
complication rate of the diagnostic and definitive procedure (i.e., radiofrequency denervation), the falsenegative rate of diagnostic injections, and the cost
effectiveness, including dropout rate, of performing
an additional diagnostic injection. With the exception
of a very low (⬍ 5%) incidence of neuritis183 that can
be reduced even further with the preemptive use of
steroid or pentoxifylline,184 the complication rate is
similar for diagnostic facet blocks and radiofrequency
denervation. In a systematic study of the cost-effectiveness of using controlled facet blocks, Bogduk and
Holmes185 determined that the use of placebo-controlled injections cannot be justified in the United
States based on financial considerations. Considering
that a substantial percentage of patients will respond
with long-term pain relief even to sham denervation,159,160 it is unlikely that the routine use of confirmatory facet blocks will become standard of care
anytime soon.
Treatment
Conservative Treatment and Pharmacotherapy
The treatment of l-z joint pain ideally consists of a
multimodal approach comprising conservative therapy,
medical management, procedural interventions, and if
indicated, psychotherapy. There are no clinical studies
specifically assessing pharmacotherapy or noninterventional treatment for lumbar facet arthropathy, although
there are several controlled studies evaluating conservative treatment for axial LBP. Tailored exercise programs
and yoga have been shown to reduce pain and prevent
relapses in patients with chronic LBP.186 –190 In randomized, clinical trials, osteopathic manipulation has been
shown to provide moderate relief for LBP patients,191,192
although one study showed no difference between the
benefits afforded by true and sham manipulation.193 Acupuncture has also been shown in randomized trials to
provide significant benefit in patients with chronic
LBP.194 –196 However, similar to manipulation, one of the
largest and most methodologically sound studies found
no difference between true and sham acupuncture.197
Nonsteroidal antiinflammatory drugs and acetaminophen are widely considered first line drugs for the treatment of LBP, with little evidence to support one particular drug over another.198 –200 Adjuvants have also been
shown to be effective in relieving LBP. In a comprehensive review on published clinical trials evaluating pharmacotherapy in LBP, Schnitzer et al.201 found strong
evidence to support the use of antidepressants for
chronic LBP, and muscle relaxants in acute back pain.
Numerous studies have also provided incontrovertible
evidence that untreated psychopathology can adversely
affect LBP treatment outcomes. In a study by Polatin et
al.202 conducted in 200 chronic LBP patients, the authors found that 77% met lifetime criteria and 59% demonstrated current symptoms for at least one psychiatric
diagnosis, with the most common being depression,
substance abuse, and anxiety disorders. Most, but not all
studies, have shown untreated psychopathology to negatively impact LBP treatment outcomes.203 In the only
study assessing the influence of psychopathology on l-z
joint interventions, Lilius et al.204 found a strong correlation between a negative response to intraarticular and
periarticular LA and steroid injections and inappropriate
signs and symptoms. We believe that the optimal management of l-z joint pain should encompass both interventional and noninterventional treatment, although clinicians are encouraged to exercise caution when
extrapolating the results of studies conducted in patients
with nonspecific LBP to those with clear-cut facet pathology.
Intraarticular Steroid Injections
The use of intraarticular steroid injections to treat l-z
joint pain is a controversial subject. In uncontrolled
studies, the long-term relief of back pain after intraarticular steroid injection ranges from 18% to 63%, with
most of these studies being conducted in patients who
did not undergo previous diagnostic l-z
blocks.118 –120,123,124,144,205 Studies have also reported
intermediate-term pain relief after intraarticular LA
alone,142 normal saline,206,207 and hyaluronic acid.208
In the controlled trials that do exist, the results are
mixed (table 7). In the largest study, Lilius207 reported
no significant difference in outcomes between 109 patients who received large-volume (8 ml) LA and steroid
injected into l-z joints or around l-z joints or intraarticular
saline injections. In a randomized, controlled study comparing intraarticular steroid and saline in 97 patients
605
Table 7. Prospective, Clinical Trials Evaluating Intraarticular Steroid Injections for Lumbar Facet Joint Pain
Author, Year,
Methodologic Score
268
Lynch and Taylor,
1986;
MQ score ⫽ 0
Lilius et al.,207 1989;
MQ score ⫽ 1
accompanied by paraspinal
tenderness and pain worsened by
hyperextension underwent
attempted intraarticular steroid
injections at 2 most caudal l-z
joints. Failed “extraarticular”
injections designated as “control”
group.
109 pts with unilateral chronic LBP
rec’d 8 ml LA and steroid injected
into 2 l-z joints (n ⫽ 28), around 2
joints (n ⫽ 39), or 8 ml NS into 2
joints (n ⫽ 42).
Results
Comments
Relief of pain at 2 wk and 6 mo was
better in pts who had 2
intraarticular injections than the
other groups. Pts who had 1
intraarticular injection had better
relief than those who had no
successful injections.
Flaws include lack of randomization,
poor outcome assessment, failure
to identify pts based on
diagnostic injections, and failure
to blind the examining physician.
All 3 groups demonstrated significant
improvement in pain scores (at 3
mo), disability scores, clinical
examination findings, and return to
work at 6 wk after injection. No
differences were noted on any
variable between groups.
Pts were not diagnosed with l-z
joint pain before injection. Large
volumes used rendered injections
nonspecific. Large SDs were
found for variables measured.
Other flaws include suboptimal
outcomes measures and lack of a
blinded observer. Pain scores
measured at 3 mo by
questionnaire.
11 pts lost to follow-up. Flaws
include not using l-z joint blocks
for diagnosis, lack of a blinded
observer, poor outcome
measures, and no true control
group.
Differences between groups at 6 mo
reduced when cointerventions
taken into account. Although this
is the only study that identified
study pts based on diagnostic
injections, these injections were
not “controlled.” NS is known to
provide pain relief ⬎ that
expected from placebo.
Flaws include no true control group,
failure to identify pts based on
diagnostic injections, no
monitoring of cointerventions,
lack of a blinded observer, and
poor outcome assessment.
Inclusion criteria included at least
moderate facet degeneration on
radiologic imaging. Flaws include
lack of a control group, failure to
identify pts based on diagnostic
injections, no monitoring of
cointerventions, and multiple
injections.
Differences remained significant at 3
mo but not 6 mo after injection.
Pain scores obtained by mailed
questionnaire. No functional
assessment done. Use of SPECT
was cost effective.
Nash,156 1990; MQ
score ⫽ 2
67 pts with chronic LBP were
randomly assigned by pairs to
receive either 1.5 ml intraarticular
LA and steroid or MBB with 2 ml
LA.
At 1-mo follow-up, 12 pairs reported
MBB to be more beneficial, 11
reported intraarticular injection to
be better, and 3 reported no
difference.
Carette et al.,206
1991;
MQ score ⫽ 5
97 pts with chronic LBP who reported
immediate relief after LA facet
injections rec’d either 2 ml steroid
and saline (n ⫽ 49) or saline (n ⫽
48) into L4–L5 and L5–S1 l-z joints.
Marks et al.,8 1992;
MQ score ⫽ 3
randomly assigned to receive either
1.5 ml steroid and LA MBB or
intraarticular injections (2 ml at
lowest level).
42% of pts who received steroid and
33% who rec’d placebo reported
marked improvement for up to 3
mo (P ⫽ not significant). At 6 mo,
the steroid group reported less pain
and disability. Only 22% of pts in
steroid group and 10% in placebo
group had sustained improvement
through 6 mo.
Pts who had facet joint injections had
better pain relief than those who
had MBB at all follow-up visits up
to 3 mo, but this was only
significant at 1-mo review.
Fuchs et al.,208 2005;
MQ score ⫽ 1
randomly assigned to receive either
1 ml HA or steroid into the 3 lowest
facet joints at weekly intervals ⫻ 6.
Pneumaticos et
al.,215 2006;
MQ score ⫽ 3
47 pts with chronic LBP worse with
lumbar extension and radiologic
evidence of l-z joint abnormalities
were randomly assigned in a 2:1
ratio to undergo intraarticular LA
and steroid injections (3 ml) based
on SPECT scans or physical
examination.
Pts who rec’d HA injections
experienced a 40% decrease in
pain scores vs. a 56% reduction in
those who rec’d steroid (P ⫽ not
significant). Greatest pain reduction
observed 3 mo after treatment in
HA group and 1 wk after treatment
in steroid group.
1 mo after injection, 87% of pts with
(⫹) SPECT had significant pain
improvement vs. 12.5% of pts with
(⫺) SPECT and 31% of pts who
underwent injections based on
physical examination.
Methodologic quality (MQ) score based on the 5-point Jadad scale.275 A score of ⱖ 3 indicates high methodologic quality.
HA ⫽ hyaluronic acid; LA ⫽ local anesthetic; LBP ⫽ low back pain; l-z ⫽ lumbar zygapophysial; MBB ⫽ medial branch block; NS ⫽ normal saline; pts ⫽ patients;
SPECT ⫽ single photon emission computed tomography.
with chronic LBP, Carette et al. found a statistically
significant benefit favoring steroid only at 6 months after
the procedure.206 This study is the second largest and
most methodologically sound study evaluating intraarticular steroids, and the only one that prescreened study
patients based on diagnostic facet blocks. One flaw in
these studies is that most used saline injections as the
control group, and normal saline has been shown to
provide better pain relief than that expected with a true
placebo for a multitude of invasive procedures.209 –211 In
five recent review articles, the authors were split as to
whether intraarticular steroids constituted an effective
treatment for l-z joint pain, with three concluding they
did not.128,181,212–214 Based on the existing evidence,
including basic science studies demonstrating inflammatory mediators to be present in and around degenerated
facet joints,43,44 we believe that intraarticular steroid
injections may provide intermediate-term relief to a
small subset of patients with l-z joint pain accompanied
by an active inflammatory process. Evidence to support
this assertion is bolstered by several recent prospective
and observational studies evaluating low- to intermediate-volume (1–3 ml) LA and steroid intraarticular l-z joint
injections performed in more than 160 patients with
606
axial LBP.150,215,216 In these studies, patients with positive single photon emission computed tomography experienced dramatically better pain relief (⬎ 75% success
rate) compared with those with negative or no single
photon emission computed tomography (⬍ 40% success
rate) up to 3 months after injection. In the two studies
that followed patients for 6 months after injection, the
beneficial effect wore off after the 3-month evaluation.150,215 Radionuclide bone scintigraphy is capable of
depicting synovial changes caused by inflammation, degenerative changes associated with bone remodeling,
and increased metabolic function. In addition to radiologic evidence of joint inflammation and degeneration,
intraarticular steroid injections may be more effective in
those patients who obtain definitive pain relief after a
diagnostic screening block, and when LA is added to the
injectate.
Radiofrequency Denervation
In 1971, Rees18 first described percutaneous denervation as an effective new treatment for discogenic back
pain. Notwithstanding his greater than 99% reported
success rate, it remains a subject of controversy as to
whether his technique actually achieved “facet rhizolysis,” since the instrument he used may not have been
long enough to accomplish anything more than a myofasciotomy.3 The technique as practiced today, which
entails using radiofrequency energy channeled through a
small-diameter needle to create a controlled burn that
severs the l-z joint nerve supply, is generally credited to
Shealy, who was motivated by what he perceived to be
an unacceptably high incidence of local hemorrhagic
complications.19,20 Subsequently, it has been used with
varying degrees of success to treat different forms of
spinal pain, including whiplash,217 sacroiliac joint
pain,218,219 discogenic pain,220 and intractable sciatica.221 There are literally dozens of uncontrolled trials
touting the benefits of radiofrequency denervation for l-z
joint pain,222 with most reporting sustained relief in
50 – 80% of subjects without previous back surgery19,223–
228 and 35–50% of patients with failed back surgery
syndrome.153,229 –232
Only five placebo-controlled studies have been conducted evaluating radiofrequency denervation for l-z
joint pain (table 8). In the first study, King and Lagger3
randomly assigned 60 patients with low back and leg
pain to receive empirical (without stimulation) radiofrequency denervation of the dorsal rami, a radiofrequency
lesion made in the muscle, or a sham lesion after electrical stimulation. At their 6-month follow-up, 27% of
patients in the facet denervation group experienced satisfactory pain relief versus 53% in the myotomy group
and 0% in the sham group. The main criticism in this
study is that no diagnostic blocks were performed to
screen people for l-z joint pain. More than 15 yr later,
Gallagher et al.158 randomly assigned 41 patients based
on their response to diagnostic intraarticular blocks
(equivocal or good response) to either sham or true
denervation. A statistically significant difference in outcomes was observed at 1 month only between sham and
true radiofrequency denervation in those patients who
obtained a definitive response to diagnostic blocks. This
difference persisted for the duration of the 6-month
follow-up. In the smallest but most methodologically
sound233 study among the five controlled trials, van
Kleef et al.157 found a 46% pain reduction in the radiofrequency lesion group versus an 8% reduction in the
placebo group. At 12-month follow-up, 7 of 15 patients
in the radiofrequency group continued to have a successful outcome versus only 2 of 16 in the sham group.
Leclaire et al.159 conducted a placebo-controlled study in
70 patients with a putative diagnosis of facet arthropathy. At their 4-week follow-up, the only outcome variable that favored the treatment group was an improvement in mean Roland-Morris disability score. At 12
weeks, no difference was noted between groups for pain
levels or any measure of functional capacity. The key
flaw in this study is that the authors used “significant
pain relief lasting ⬎ 24 h” after an intraarticular injection
of LA and steroid as their main inclusion criterion. In
addition to being ambiguous, the 24-h threshold is inconsistent with the pharmacodynamics of lidocaine. In
the largest controlled study evaluating radiofrequency
denervation, van Wijk et al.160 found the only difference
between the treatment and control group at 3 months
was that more radiofrequency patients reported a 50% or
greater diminution in back pain than sham patients (62%
vs. 39%). For mean reduction in VAS pain scores, change
in analgesic intake, and functional assessments, no differences were noted between groups.
The chief criticisms of these studies (see table 8 for
more details) include suboptimal needle positioning and
not selecting study patients based on placebo-controlled
or comparative LA blocks. In the only prospective study
to evaluate radiofrequency outcomes in patients selected
based on concordant response to serial LA blocks, Dreyfuss et al.182 reported that 87% of 15 patients obtained at
least 60% pain relief 12 months status post radiofrequency denervation, with 60% of patients achieving at
least 90% relief. In addition to stringent inclusion criteria, the authors used 16-gauge electrodes and assessed
the efficacy of radiofrequency denervation by performing electromyography of the multifidus muscles.
Whereas some may construe these findings as evidence that radiofrequency denervation is a fundamentally flawed treatment, a more plausible interpretation is
that they indicate a strong need to optimize radiofrequency denervation techniques and better identify those
candidates who are likely to obtain positive outcomes.
Several investigators have determined that placing the
electrode parallel rather than perpendicular to the target
nerve substantially increases the size of the lesion,
607
Table 8. Outcomes for Randomized, Controlled Studies Assessing Medial Branch Radiofrequency Denervation for Facet Joint Pain
Author, Year
Number and Type of Patients
King and Lagger,3 1976
60 pts with chronic low back
and leg pain and paraspinal
tenderness were randomly
assigned to 3 groups. Group
I had RF denervation of the
primary posterior ramus,
group II had RF performed
using a 1.25-inch needle
inserted within the area of
maximum tenderness
(assumed to be a myotomy),
and group III rec’d
stimulation but no
coagulation (control).
Subjects were 41 pts with
chronic LBP who obtained
“clear-cut or equivocal” relief
from single intraarticular
facet joint injections with LA
and steroid. 18 pts with a
good response and 6 pts
with an equivocal response
underwent RF denervation.
12 pts with a good response
and 5 with an equivocal
response underwent sham
denervation.
chronic LBP who
after a single MBB (1
dropout). Compared true
denervation with sham.
Gallagher et al.,158 1994
van Kleef et al.,157 1999
Sanders and
Zuurmond,276 1999
Leclaire et al.,159 2001
van Wijk et al.,160 2005
chronic LBP who
obtained ⱖ 50% after single
intraarticular injection with
lidocaine. Half of the pts
rec’d medial branch RF
denervation, and half rec’d
intraarticular denervation.
chronic LBP who obtained
“significant” pain relief
lasting ⬎ 24 h after single
intraarticular facet injection
with lidocaine and steroid (4
dropouts). Compared true
81 pts with chronic LBP who
after 2-level intraarticular
facet injection with LA (no
dropouts). Compared true
Follow-up Period and
Methodologic Scores
Results
Comments
6 mo; MQ ⫽ 2; CR ⫽ 5
In group I, 27% had ⱖ 50%
relief at 6 mo vs. 53% in
group II and 0% in group
III.
Did not use diagnostic blocks
before randomization. Likely
included many pts with
sciatica. In some pts, 1.25
inches may be sufficient to
reach the medial branch.
Used 120-s lesion; 3 lesions
were empirically made
without electrical stimulation.
Electrode not placed parallel
to nerve.
6 mo; MQ ⫽ 2; CR ⫽ 6
Significant differences in
pain scores noted only
between patients with a
good response to LA
blocks who underwent
true RF denervation (n ⫽
18) and those with a good
response who underwent
sham treatment (n ⫽ 12).
Differences were noted 1
and 6 mo after
procedures.
Did not define “good” or
“equivocal” response to
diagnostic injections.
Anatomical landmarks not
well described. Observer not
blinded. Electrode not
placed parallel to nerve. In
Methods, stated only LA
used, but in abstract, stated
LA and steroid were used.
Used 90-s lesions.
12 mo; MQ ⫽ 5; CR ⫽
8
After 3 mo, 9 of 15 pts in
lesion group vs. 4 of 16 in
sham group had ⱖ 50%
pain relief. At 1-yr followup, 7 of 15 in lesion group
and 2 of 16 in sham group
had ⱖ 50% relief.
Both groups improved at 3
mo, but intraarticular
denervation group
improved more than
medial branch RF group.
Used 0.75 ml injectate for
diagnostic blocks. Electrode
not placed perpendicular to
target nerve. Used multifidus
rather than sensory
stimulation to identify medial
branch. Used 60-s lesions.
Used 1 ml for diagnostic
blocks. Medial branch
lesions done at inferolateral
aspect of facet capsule and
upper border of transverse
process. 3 intraarticular facet
lesions done. Used 60-s
lesions.
Did not define “significant pain
relief” with diagnostic
injection. Inclusion criteria
of ⬎ 24 h pain relief is
inconsistent with
pharmacology of lidocaine.
Performed 2 lesions, each
for 90 s. Anatomical
landmarks not noted.
Electrode not placed parallel
to nerve.
Blinding ended at 3 mo
in ⬎ 70% of pts.
Improvement in pain scores
persisted throughout 12-mo
follow-up. Used 60-s lesions.
3 mo; MQ ⫽ 1; CR ⫽ 6
12 wk; MQ ⫽ 4; CR ⫽
8
At 4 wk, there were modest
improvements in RolandMorris (P ⫽ 0.05) and VAS
pain scores (P ⫽ not
significant), but not
Oswestry score. No
difference in any outcome
measure at 12 wk.
12 mo; MQ ⫽ 5; CR ⫽
7
Combined outcome measure
(pain score, physical
activity, and analgesic
intake) showed no
differences between
groups at 3 mo. VAS pain
score improved in both
groups at 3 mo. Global
perceived effect was
greater in treatment than
sham group at 3 mo.
Methodologic quality (MQ) score based on the 5-point Jadad scale. 275 A score of ⱖ 3 indicates high methodologic quality. Clinical relevance (CR) score based
on patient selection parameters and radiofrequency (RF) technique description (0 –9 scale) as described by Geurts et al.233
LA ⫽ local anesthetic; LBP ⫽ low back pain; MBB ⫽ medial branch block; pts ⫽ patients; rec’d ⫽ received; VAS ⫽ visual analog scale.
thereby reducing the likelihood the treatment will miss
or only partially coagulate the target nerve.234,235 After a
literature review and cadaveric study, Lau et al.234 concluded the ideal electrode position is across the lateral
neck of the superior articular process rather than the
groove formed at the angle of the superior articular and
transverse processes, as was used in most studies.159,160
Other investigators have found the maximal lesion size
to be reached within 60 s of lesion time,235–237 indepenAnesthesiology, V 106, No 3, Mar 2007
dent of whether the system is temperature or voltagecontrolled.238 Studies conducted in human myocardium
have determined that irrigation fluid has either no effect
or a slightly beneficial effect on lesion size.239 Hence, the
use of LA to prevent procedure-related pain or steroid to
reduce the incidence of neuritis184 should theoretically
have no adverse effects on the efficacy of radiofrequency
denervation.
Another flaw that pervades most radiofrequency stud-
608
ies is that sensory stimulation (usually at ⱕ 0.5 V) is used
to corroborate proximity of the electrode to the targeted
medial branch. Whereas sensory stimulation is almost
certain to be perceived when the electrode is placed on
or adjacent to a neural structure, it is our experience that
many patients perceive concordant sensory stimulation
at 0.5 V or less, even when the electrode is purposefully
placed in muscle, as during sham procedures. An attractive alternative to sensory stimulation is to instead (or in
addition) attempt to elicit multifidus muscle contraction,
because the same medial branch that innervates the
facet joint also innervates this paraspinal muscle. In the
two studies in which the medial branch was identified
by motor stimulation of the multifidus muscle, both
reported positive outcomes.157,182
In a large, multicenter outcome study, Cohen et al.153
attempted to identify factors associated with successful
radiofrequency treatment in 192 patients who underwent denervation at three teaching hospitals after a
single, positive MBB. Among the 15 variables analyzed
for their association with treatment outcome, only
paraspinal tenderness was found to predict a successful
treatment. Factors associated with failed treatment included increased pain with hyperextension and axial
rotation (i.e., facet loading), duration of pain and previous back surgery. The latter two variables have been
associated with treatment failure not only for radiofrequency denervation, but a host of other LBP interventions as well, including epidural steroid injections and
open surgery.240 –242 When pain returns after radiofrequency denervation, which typically occurs between 6
months and 1 yr, repeated neurotomy can be performed
with no diminution in efficacy.243 In addition to continuous, high-temperature radiofrequency medial branch
ablation, pulsed radiofrequency (2– 6 months of effective pain relief),244 cryodenervation (3– 6 months of pain
relief),245–248 and phenol neurolysis249,250 have also
been reported to provide intermediate to long-term pain
relief in uncontrolled studies.
Complications after Intraarticular Injections and
Radiofrequency Denervation
Serious complications and side effects are extremely
uncommon after facet interventions. The metabolic and
endocrine sequelae of intrafacetal depot steroids have
not been studied, but extrapolating from epidural steroid
injections, one would expect suppression of the hypothalamic–pituitary–adrenal axis lasting up to 4 weeks
depending on the depot steroid used, and impaired insulin sensitivity manifesting as elevated glucose levels for
less than a week.251,252 Although rare, a host of infections have been reported after intraarticular injections
including septic arthritis, epidural abscess, and meningitis.253–255 Case reports of spinal anesthesia and postdural
puncture headache have also been published.256,257
Numbness and/or dysesthesias have been reported afAnesthesiology, V 106, No 3, Mar 2007
ter radiofrequency denervation but tend to be transient
and self-limiting.219,258 Burns are rare with radiofrequency procedures and may result from electrical faults,
insulation breaks in the electrodes, and generator malfunction.19,226,259 The most common complication after
facet joint radiofrequency is neuritis, with a reported
incidence of less than 5%.183 In one study, the administration of corticosteroid or pentoxifylline was found to
reduce the incidence of postprocedure pain after radiofrequency denervation.184 There is also a theoretical risk
of thermal injury to the ventral rami if an electrode slips
ventrally over the transverse process.
Surgery
Surgery is occasionally performed to treat facet arthropathy despite a lack of evidence supporting fusion
for degenerative spinal disorders.260,261 Not surprisingly, the results of studies evaluating the use of l-z
joint blocks to predict lumbar arthrodesis outcomes
are discouraging (table 9). In the three studies that
compared surgical outcomes between facet block responders and nonresponders, all three failed to show
a difference between groups.262–264 Bough et al.138
conducted a retrospective review of 127 facet joints
surgically removed from 84 patients in an attempt to
correlate histologic evidence of facet degeneration
with provocative response to preoperative facet arthrography. Although the authors found the positive
predictive value of concordant pain reproduction to
be 85%, the negative predictive value was only 43%,
leading them to conclude that provocative facet arthrography was of little value as a presurgical screening tool. In a prospective case series, Lovely and
Rastogi265 found that 83% of 23 patients who responded to bracing and three successive facet blocks
achieved at least 90% pain relief after fusion surgery at
the latest follow-up. However, the large volumes used
per block, the failure to exclude placebo-responders,
and the lack of any comparison group undermine the
conclusions that can be drawn. One reason patients
with l-z joint pain might respond to arthrodesis is
because some surgeons, either purposefully or inadvertently, perform medial branch rhizotomies during
pedicle screw placement. In summary, there is no
convincing evidence to support any surgical intervention for l-z joint pain aside from that resulting from a
traumatic dislocation.
Conclusions
Pain originating from the l-z joints has long been recognized as a potential source of LBP. Anatomical studies
suggest that with aging, the facet joints become weaker
and their orientation changes from coronal to sagittal
609
Table 9. Studies Evaluating the Ability of Lumbar Facet Blocks to Predict Operative Results
Author, Year
Patients and Methods
Results
Comments
263
Prospective study evaluating the
value of external fixation to
predictive fusion outcome in 35
pts. 14 pts underwent
preoperative facet blocks.
Among the 9 pts who reported
temporary relief from facet
blocks, 5 experienced relief
from external fixation. In the 5
pts who had no relief with
facet blocks, 4 experienced
relief after fixation.
The specificity of pain
provocation for facet disease
was 75%, sensitivity 59%,
positive predictive value 85%,
and negative predictive value
43%. The authors concluded
symptom provocation during
facet arthrography was of little
value as a surgical screening
tool.
Both groups improved after
fusion. The 26 pts who
responded favorably to facet
injections did no better
clinically than the 10 pts who
did not.
15% of pts had complete relief,
41% partial relief, and 44% no
relief after l-z joint blocks.
Response to facet blocks not
predictive of surgical or
nonsurgical success.
Fusion was technically
successful 77% of time. 83%
of pts reported ⱖ 90% relief,
and 13% reported partial
relief.
Study not designed to assess
value of facet blocks in
predicting outcome of
spinal fixation.
Esses et al.,
1989
Bough et al.,138 1990
Retrospective study comparing
results of surgical pathology
and preoperative provocative
facet arthrography in 84 pts
who underwent spinal fusion.
Jackson,262 1992
Retrospective review involving 36
pts who underwent
posterolateral lumbar fusion
after facet injections.
Esses and Moro,264 1993
Retrospective review involving the
results of spinal fusion (n ⫽ 82)
and nonoperative treatment (n
⫽ 44) in 126 pts who
underwent facet blocks.
Lovely and Rastogi,265
1997
Prospective case series involving
91 pts who responded to
bracing and underwent 197
facet blocks. 28 pts who
obtained ⬎ 70% pain relief on 3
separate occasions underwent
spinal fusion.
Histopathology results
reviewed for 127 l-z joints.
Clinical outcomes not
discussed.
Mean follow-up 6.1 yr.
Response to injection not a
consideration for fusion.
296 pts underwent facet
blocks during index period,
but only 126 had follow-up
(mean 4.6 yr.
Mean follow-up 32 mo. No
comparison group who
either failed or did not
receive preoperative l-z
joint blocks. Used 3–5 ml
injectate per facet level.
l-z ⫽ lumbar zygapophysial; pts ⫽ patients.
positioning, predisposing them to injury from rotational
stress. The three most caudal facet joints, L3–L4, L4 –L5,
and L5–S1, are exposed to the greatest strain during
lateral bending and forward flexion and are thus more
prone to repetitive strain, inflammation, joint hypertrophy, and osteophyte formation. Osteoarthritis of the
facet joints is commonly found in association with degenerative disc disease. The exact prevalence of facet
disease resulting in axial LBP is unclear but may be as
high as 10 –15% of patients.
There are no discrete historic and physical findings
pathognomonic for lumbar facet arthropathy. The referral patterns for pain arising from the lumbar facet
joints at different levels overlap considerably. In addition to axial LBP, pathology arising from the lower
facet joints is associated with referred pain to the
buttock, thigh, groin, and sometimes lower leg,
whereas that referred from the upper lumbar facet
joints extends into the flank, hip, groin, and lateral
thigh. Reports on the correlation between CT and MRI
evidence of facet arthropathy and the response to
diagnostic lumbar facet blocks are conflicting. Because the facet joint is innervated by the medial
branches arising from the posterior rami of the spinal
nerve at the same level and a level above the joint, LA
blocks of these nerves have been advocated for diagnostic and prognostic purposes. Intraarticular l-z joint
injection with LA has also been proposed as a method
for diagnosing facet joint pain, with both procedures
appearing to provide comparable diagnostic value. As
with other blocks, the potential for false positive and
false negative responses must be considered, and
steps should taken to reduce their incidence.
In addition to providing short and occasionally intermediate-term pain relief, diagnostic blocks are considered predictive of the potential usefulness of subsequent
neurolytic procedures such as radiofrequency denervation. In carefully selected patients who fail conservative
treatments such as physical and pharmacologic therapies, intraarticular steroid injections and radiofrequency
denervation are treatment options. Studies evaluating
the long-term outcomes from these procedures have
610
thus far provided conflicting evidence. The results of
surgical therapies including arthrodesis for facet arthropathy are discouraging.
The authors thank Paul Dreyfuss, M.D. (Professor of Physical Medicine and
Rehabilitation, University of Washington School of Medicine, Seattle, Washington), for his review of the manuscript.
References
1. Manchikanti L: The growth of interventional pain management in the new
millennium: A critical analysis of utilization in the Medicare population. Pain
Physician 2004; 7:465–82
2. Lewin T, Moffett B, Vidik A: The morphology of the lumbar synovial
intervertebral joints. Acta Morphol Neerl Scand 1962; 4:299–319
3. King JS, Lagger R: Sciatica viewed as a referred pain syndrome. Surg Neurol
1976; 5:46–50
4. Borenstein D: Does osteoarthritis of the lumbar spine cause chronic low
back pain? Curr Pain Headache Rep 2004; 8:512–7
5. Cavanaugh JM, Ozaktay AC, Yamashita HT, King AI: Lumbar facet pain:
Biomechanics, neuroanatomy and neurophysiology. J Biomechanics 1996; 29:
1117–29
6. Stillwell DL: The nerve supply of the vertebral column and its associated
structures in the monkey. Anat Rec 1956; 125:136–69
7. Hirsch C, Ingelmark BE, Miller M: The anatomical basis for low back pain:
Studies on the presence of sensory nerve endings in ligamentous, capsular and
intervertebral disc structures in the human lumbar spine. Acta Orthop Scand
1963; 33:1–17
8. Marks RC, Houston T, Thulbourne T: Facet joint injection and facet nerve
block: A randomized comparison in 86 patients with chronic low back pain. Pain
1992; 49:325–8
9. Mooney V, Robertson J: The facet syndrome. Clin Orthop Relat Res 1976;
115:149–56
10. McCall IW, Park WM, O’Brien JP: Induced pain referral from posterior
lumbar elements in normal subjects. Spine 1979; 4:441–6
11. Kuslich SD, Ulstrom CL, Michael CJ: The tissue origin of low back pain and
sciatica: A report of pain response to tissue stimulation during operations on the
lumbar spine using local anesthesia. Orthop Clin North Am 1991; 22:181–7
12. Schwarzer AC, Aprill CN, Derby R, Fortin J, Kine G, Bogduk N: Clinical
features of patients with pain stemming from the lumbar zygapophysial joints: Is
the lumbar facet syndrome a clinical entity? Spine 1994; 19:1132–7
13. Goldthwaite JE: The lumbosacral articulation: An explanation of many
cases of lumbago, sciatica, and paraplegia. Boston Med Surg J 1911; 164:365–72
14. Putti V: New concepts in the pathogenesis of sciatica pain. Lancet 1927;
2:53–60
15. Ghormley RK: Low back pain with special reference to the articular facets,
with presentation of an operative procedure. JAMA 1933; 101:1773–7
16. Mixter WJ, Barr JS: Rupture of the intervertebral disc with involvement of
the spinal canal. N Engl J Med 1934; 211:210–5
17. Badgley CE: The articular facets in relation to low back pain and sciatic
radiation. J Bone Joint Surg (Am) 1941; 23:481–96
18. Rees WE: Multiple bilateral subcutaneous rhizolysis of segmental nerves in
the treatment of the intervertebral disc syndrome. Ann Gen Pract 1971; 26:126–7
19. Shealy CN: Percutaneous radiofrequency denervation of spinal facets:
Treatment for chronic back pain and sciatica. J Neurosurg 1975; 43:448–51
20. Shealy CN: Facet denervation in the management of back and sciatic pain.
Clin Orthop 1976; 115:157–64
21. Glover JR: Arthrography of the joints of the lumbar vertebral arches.
Orthop Clin North Am 1977; 8:37–42
22. Yahia LH, Garzon S: Structure on the capsular ligaments of the facet joints.
Ann Anat 1993; 175:185–8
23. Cyron BM, Hutton WC: The tensile strength of the capsular ligaments of
the apophyseal joints. J Anat 1981; 132:145–50
24. Bogduk N: Clinical Anatomy of the Lumbar Spine and Sacrum, 3rd edition.
Edinburgh, Churchill Livingstone, 1997, pp 33– 42
25. Pedersen HE, Blunck CF, Gardner E: The anatomy of the lumbosacral
posterior rami and meningeal branches of spinal nerves (sinuvertebral nerves)—
with an experimental study of their function. J Bone Joint Surg (Am) 1956;
38:377–91
26. Bogduk N: Clinical Anatomy of the Lumbar Spine and Sacrum, 3rd edition.
Edinburgh, Churchill Livingstone, 1997, pp 127– 44
27. Maigne JY, Maigne R, Guerin-Surville H: The lumbar mamillo-accessory
foramen: A study of 203 lumbosacral spines. Surg Radiol Anat 1991; 13:29–32
28. Bogduk N, Tynan W, Wilson AS: The nerve supply to the human lumbar
intervertebral discs. J Anat 1981; 132:39–56
29. Bogduk N, Wilson AS, Tynan W: The human lumbar dorsal rami. J Anat
1982; 134:383–97
30. Bogduk N: The innervation of the lumbar spine. Spine 1983; 8:286–93
31. Dreyfuss P, Schwarzer AC, Lau P, Bogduk N: Specificity of lumbar medial
branch and L5 dorsal ramus blocks: A computed tomography study. Spine 1997;
22:895–902
32. Kaplan M, Dreyfuss P, Halbrook B, Bogduk N: The ability of lumbar medial
branch blocks to anesthetize the zygapophysial joint: A physiologic challenge.
Spine 1998; 23:1847–52
33. Paris SV: Anatomy as related to function and pain. Orthop Clin North Am
1983; 14:475–89
34. Jerosch J, Castro WH, Liljenqvist U: Percutaneous facet coagulation: Indication, technique, results, and complications. Neurosurg Clin North Am 1996;
7:119–34
35. Emminger E: Les articulations interapophysaires et leurs structures meniscoides vue sous l’angle de la pathologie. Ann Med Physique 1972; 15:219–38
36. Pedersen HE, Blunck CF, Gardner E: The anatomy of lumbosacral posterior
rami and meningeal branches of spinal nerves (sinuvertebral nerves). J Bone Joint
Surg (Am) 1956; 38:377–91
37. Suseki K, Takahashi Y, Takahashi K, Chiba T, Tanaka K, Morinaga T,
Nakamura S, Moriya H: Innervation of the lumbar facet joints: Origins and
functions. Spine 1997; 22:477–85
38. Ashton IK, Ashton BA, Gibson SJ, Polak JM, Jaffray DC, Eisenstein SM:
Morphological basis for back pain: The demonstration of nerve fibers and neuropeptides in the lumbar facet joint capsule but not in ligamentum flavum.
J Orthop Res 1992; 10:72–8
39. El-Bohy AA, Cavanaugh JM, Getchell ML, Bulas T, Getchell TV, King AI:
Localization of substance P and neurofilament immunoreactive fibers in the
lumbar facet joint capsule and supraspinous ligament of the rabbit. Brain Res
1988; 460:379–82
40. Beaman DN, Graziano GP, Glover RA, Wojtys EW, Chang V: Substance P
innervation of lumbar spine facet joints. Spine 1993; 18:1044–9
41. Giles LG: Human lumbar zygapophyseal joint inferior recess synovial folds:
A light microscope examination. Anat Rec 1988; 220:117–24
42. Giles LG, Taylor JR: Innervation of lumbar zygapophyseal joint synovial
folds. Acta Orthop Scand 1987; 58:43–6
43. Willburger RA, Wittenberg RH: Prostaglandin release from lumbar disc and
facet joint tissue. Spine 1994; 19:2068–70
44. Igarashi A, Kikuchi S, Konno S, Olmarker K: Inflammatory cytokines
released from the facet joint tissue in degenerative lumbar spinal disorders. Spine
2004; 29:2091–5
45. Horwitz T, Smith RM: An anatomical, pathological and roentgenological
study of the intervertebral joints of the lumbar spine and of the sacroiliac joints.
Am J Roentgenol 1940; 43:173–86
46. Masharawi Y, Rothschild B, Dar G, Peleg S, Robinson D, Been E, Hershkovitz I: Facet orientation in the thoracolumbar spine: Three-dimensional anatomic and biomechanical analysis. Spine 2004; 29:1755–63
47. Panjabi MM, Oxland T, Takata K, Goel V, Duranceau J, Krag M: Articular
facets of the human spine: Quantitative three-dimensional anatomy. Spine 1993;
18:1298–1310
48. Grobler LJ, Robertson PA, Novotny JE, Pope MH: Etiology of spondylolisthesis: Assessment of the role played by lumbar facet joint morphology. Spine
1993; 18:80–91
49. Boden SD, Riew KD, Yamaguchi K, Branch TP, Schellinger S, Wiesel SW:
Orientation of the lumbar facet joints: Association with degenerative disc disease.
J Bone Joint Surg (Am) 1996; 78:403–11
50. Murtagh FR, Paulsen RD, Rechtine GR: The role and incidence of facet
tropism in lumbar spine degenerative disc disease. J Spinal Disord 1991; 4:86–9
51. Dai LY: Orientation and tropism of lumbar facet joints in degenerative
spondylolisthesis. Int Orthop 2001; 25:40–2
52. Farfan HF, Huberdeau RM, Dubow HI: Lumbar intervertebral disc degeneration: The influence of geometric features on the pattern of disc degeneration—a post-mortem study. J Bone Joint Surg (Am) 1972; 54:492–510
53. Cyron BM, Hutton WC: Articular tropism and stability of the lumbar spine.
Spine 1980; 5:168–72
54. Noren R, Trafimow J, Andersson GB, Huckman MS: The role of facet joint
tropism and facet angle in disc degeneration. Spine 1991; 16:530–2
55. Van Schaik JP, Verbiest H, Van Schaik FD: The orientation of laminae and
facet joints in the lower lumbar spine. Spine 1985; 10:59–63
56. Vanharanta H, Floyd T, Ohnmeiss DD, Hochschuler SH, Guyer RD: The
relationship of facet tropism to degenerative disc disease. Spine 1993; 18:1000–5
57. Yang KH, King AI: Mechanism of facet load transmission as a hypothesis
for low-back pain. Spine 1984; 9:557–65
58. Adams MA, Hutton WC: The effect of posture on the role of the apophysial
joints in resisting intervertebral compressive forces. J Bone Joint Surg (Br) 1980;
62:358–62
59. Nachemson AL: The load on lumbar discs in different positions of the
body. Clin Orthop 1966; 45:107–22
60. Lorenz M, Patwardhan A, Vanderby R Jr: Load-bearing characteristics of
lumbar facets in normal and surgically altered spinal segments. Spine 1983;
8:122–30
61. Song KJ, Lee KB: Bilateral facet dislocation on L4-5 without neurologic
deficit. J Spinal Disord 2005; 18:462–4
62. Ianuzzi A, Little JS, Chiu JB, Baitner A, Kawchuk G, Khalsa PS: Human
lumbar facet joint capsule strains: I. During physiological motions. Spine J 2004;
4:141–52
63. Little JS, Ianuzzi A, Chiu JB, Baitner A, Khalsa PS: Human lumbar facet joint
capsule strains: II. Alteration of strains subsequent to anterior interbody fixation.
Spine J 2004; 4:153–62
64. Esses SI, Doherty BJ, Crawford MJ, Dreyzin V: Kinematic evaluation of
lumbar fusion techniques. Spine 1996; 21:676–84
65. Chow DH, Luk LD, Evans JH, Leong JC: Effects of short anterior lumbar
interbody fusion on biomechanics of neighboring unfused segments. Spine 1996;
21:549–55
66. Lee CK: Accelerated degeneration of the segment adjacent to a lumbar
fusion. Spine 1988; 13:375–7
67. Lee CK, Langrana NA: Lumbosacral spinal fusion: A biomechanical study.
Spine 1984; 9:574–81
68. Quinnell RC, Stockdale HR: Some experimental observations of the influence of a single lumbar floating fusion on the remaining spine. Spine 1981;
6:263–7
69. Little JS, Khalsa PS: Human lumbar spine creep during cyclic and static
flexion: Creep rate, biomechanics, and facet joint capsule strain. Ann Biomed Eng
2005; 33:391–401
70. Little JS, Khalsa PS: Material properties of the human lumbar facet joint
capsule. J Biomech Eng 2005; 127:15–24
71. Dory MA: Arthrography of the lumbar facet joints. Radiology 1981; 140:
23–7
72. Gray DP, Bajwa ZH, Warfield CA: Facet block and neurolysis, Interventional Pain Management, 2nd edition. Edited by Waldman SD. Philadelphia, WB
Saunders, 2001, pp 446 – 83
73. Oudenhoven RC: Lumbar monoradiculopathy due to unilateral facet hypertrophy. Neurosurgery 1982; 11:726–7
74. Wilde GP, Szypryt ET, Mulholland RC: Unilateral lumbar facet joint hypertrophy causing nerve root irritation. Ann R Coll Surg Engl 1988; 70:307–10
75. Pape E, Eldevik P, Vandvik B: Diagnostic validity of somatosensory evoked
potentials in subgroups of patients with sciatica. Eur Spine J 2002; 11:38–46
76. Kang YM, Choi WS, Pickar JG: Electrophysiologic evidence for an intersegmental reflex pathway between lumbar paraspinal tissues. Spine 2002; 27:
E56–63
77. Indahl A, Kaigle A, Reikeras O, Holm S: Electromyographic response of the
porcine multifidus musculature after nerve stimulation. Spine 1995; 20:2652–8
78. Yamashita T, Cavanaugh JM, El-Bohy AA, Getchell TV, King AI: Mechanosensitive afferent units in the lumbar facet joint. J Bone Joint Surg (Am) 1990;
72:865–70
79. Yamashita T, Minaki Y, Seiichi I, Cavanaugh JM, King AI: Somatosensory
innervation of the lumbar spine and adjacent tissues. Trends Comparat Biochem
Physiol 1993; 1:219–27
80. Aramov AI, Cavanaugh JM, Ozaktay AC, Getchell TV, King AI: Effects of
controlled mechanical loading on group III and IV afferents from the lumbar facet
joint: An in vitro study. J Bone Joint Surg (Am) 1992; 74:1464–71
81. Ozaktay AC, Cavanaugh JM, Blagoev D, Getchell TV, King AI: Effects of
carrageenan induced inflammation in rabbit lumbar facet joint capsule and
adjacent tissue. Neurosci Res 1994; 20:355–64
82. Ozaktay AC, Kallakuri S, Cavanaugh JM, King AI: Phospholipase A2 induced electrophysiologic and histologic changes in rabbit dorsal lumbar spine
tissue. Spine 1995; 20:2659–68
83. Yamashita T, Cavanaugh JM, Ozaktay AC, Avramov AI, Getchell TV, King
AI: Effect of substance P on mechanosensitive units of tissues around and in the
lumbar facet joint. J Orthop Res 1993; 11:205–14
84. Cavanaugh JM, Ozaktay C, Yamashita T, Aramov A, Getchell TV, King AI:
Mechanisms of low back pain: A neurophysiologic and neuroanatomic study.
Clin Orthop Relat Res 1997; 335:166–80
85. Woolf CJ, Salter MW: Neuronal plasticity: Increasing the gain in pain.
Science 2000; 288:1765–9
86. Boszczyk BM, Boszczyk AA, Putz R: Comparative and functional anatomy
of the mammalian lumbar spine. Anat Rec 2001; 264:157–68
87. Revel ME, Listrat VM, Chevalier XJ, Dougados M, Nguyen MP, Vallee C,
Wybier M, Gires F, Amor B: Facet joint block for low back pain: Identifying
predictors of a good response. Arch Phys Med Rehabil 1992; 73:824–8
88. Revel M, Poiraudeau S, Auleley GR, Payan C, Denke A, Nguyen M, Chevrot
A, Fermanian J: Capacity of the clinical picture to characterize low back pain
relieved by facet joint anesthesia: Proposed criteria to identify patients with
painful facet joints. Spine 1998; 23:1972–6
89. Jackson RP, Jacobs RR, Montesano PX: Facet joint injection in low-back
pain: A prospective statistical study. Spine 1988; 13:966–71
90. Kirkaldy-Willis WH, Farfan FH: Instability of the lumbar spine. Clin Orthop
1982; 165:110–23
91. Farfan HF: Effects of torsion on the intervertebral joints. Can J Surg 1969;
12:336–41
92. Kirkaldy-Willis WH, Wedge JH, Yong-Hing K, Reilly J: Pathology and
pathogenesis of lumbar spondylosis and stenosis. Spine 1978; 3:319–28
93. Gottfried Y, Bradford DS, Oegema TR: Facet joint changes after chemonucleolysis induced disc space narrowing. Spine 1986; 11:944–54
94. Panjabi MM, Krag MH, Chung TQ: Effects of disc injury on mechanical
behavior of the human spine. Spine 1984; 9:707–13
95. Haher TR, O’Brien M, Dryer JW, Nucci R, Zipnick R, Leone DJ: The role of
the lumbar facet joints in spinal stability. Spine 1994; 19:2667–71
96. Adams MA, Freeman BJ, Morrison HP, Nelson IW, Dolan P: Mechanical
initiation of intervertebral disc degeneration. Spine 2000; 25:1625–36
611
97. Fujiwara A, Tamai K, Yamato M, An HS, Yoshida H, Saotome K, Kurihashi
A: The relationship between facet joint osteoarthritis and disc degeneration of
the lumbar spine: An MRI study. Eur Spine J 1999; 8:396–401
98. Schwarzer AC, Aprill CN, Derby R, Fortin J, Kine G, Bogduk N: The relative
contributions of the disc and zygapophyseal joint in chronic low back pain. Spine
1994; 19:801–6
99. de Vlam K, Mielants H, Verstaete KL, Veys EM: The zygapophyseal joint
determines morphology of the enthesophyte. J Rheumatol 2000; 27:1732–9
100. Guillaume MP, Hermanus N, Peretz A: Unusual localisation of chronic
arthropathy in lumbar facet joints after parvovirus B19 infection. Clin Rheumatol
2002; 21:306–8
101. Ball J: Enthesopathy of rheumatoid and ankylosing spondylitis. Ann
Rheum Dis 1971; 30:213–23
102. Campbell AJ, Wells IP: Pigmented villonodular synovitis of a lumbar
vertebral facet joint. J Bone Joint Surg (Am) 1982; 64:145–6
103. Smida M, Lejri M, Kandara H, Sayed M, Ben Chehida F, Ben Ghachem M:
Septic arthritis of a lumbar facet joint case report and review of the literature.
Acta Orthop Belg 2004; 70:290–4
104. Eisenstein SM, Parry CR: The lumbar facet arthrosis syndrome. J Bone
Joint Surg (Br) 1987; 69:3–7
105. Dreyfuss PH, Dreyer SJ, Herring SA: Lumbar zygapophysial (facet) joint
injections. Spine 1995; 20:2040–7
106. Fujishiro T, Nabeshima Y, Yasui S, Fujita I, Yoshiya S, Fujii H: Pseudogout
attack of the lumbar facet joint: A case report. Spine 2002; 27:E396–8
107. Hemminghytt S, Daniels DL, Williams AL, Haughton VM: Intraspinal
synovial cysts: Natural history and diagnosis by CT. Radiology 1982; 145:375–6
108. Howington JU, Connolly ES, Voorhies RM: Intraspinal synovial cysts:
10-year experience at the Ochsner Clinic. J Neurosurg 1999; 91 (suppl):193–9
109. Sabo RA, Tracy PT, Weinger JM: A series of 60 juxtafacet cysts: Clinical
presentation, the role of spinal instability, and treatment. J Neurosurg 1996;
85:860–5
110. Rapin PA, Gerster JC: Calcified synovial cysts of zygapophyseal joints.
J Rheumatol 1993; 20:767–8
111. Doyle AJ, Merrilees M: Synovial cysts of the lumbar facet joints in a
symptomatic population: Prevalence on magnetic resonance imaging. Spine
2004; 29:874–8
112. Das De S, McCreath SW: Lumbosacral fracture dislocations: A report of
four cases. J Bone Joint Surg (Br) 1981; 63:58–60
113. Fabris D, Costantini S, Nena U, Lo Scalzo V: Traumatic L5-S1 spondylolisthesis: Report of three cases and a review of the literature. Eur Spine J 1999;
8:290–5
114. Kaplan SS, Wright NM, Yundt KD, Lauryssen C: Adjacent fracture-dislocations of the lumbosacral spine: Case report. Neurosurgery 1999; 44:1134–7
115. Verlaan JJ, Oner FC, Dhert WJ, Verbout AJ: Traumatic lumbosacral dislocation: Case report. Spine 2001; 26:1942–4
116. Veras del Monte LM, Bago J: Traumatic lumbosacral dislocation. Spine
2000; 25:756–9
117. Twomey LT, Taylor JR, Taylor MM: Unsuspected damage to lumbar
zygapophyseal (facet) joints after motor-vehicle accidents. Med J Aust 1989;
151:215–7
118. Long DM, BenDebba M, Torgerson TS, Boyd RJ, Dawson EG, Hardy RW,
Robertson JT, Sypert GW, Watts C: Persistent back pain and sciatica in the United
States: Patient characteristics. J Spinal Disord 1996; 9:40–58
119. Murtagh FR: Computed tomography and fluoroscopy guided anesthesia
and steroid injection in facet syndrome. Spine 1988; 13:686–9
120. Destouet JM, Gilula LA, Murphy WA, Monsees B: Lumbar facet joint
injection: Indication, technique, clinical correlation and preliminary results.
Radiology 1982; 145:321–5
121. Lau LS, Littlejohn GO, Miller MH: Clinical evaluation of intra-articular
injections for lumbar facet joint pain. Med J Aust 1985; 143:563–5
122. Moran R, O’Connell D, Walsh MG: The diagnostic value of facet joint
injections. Spine 1988; 13:1407–10
123. Raymond J, Dumas JM: Intra-articular facet block: Diagnostic test or
therapeutic procedure? Radiology 1984; 151:333–6
124. Lewinnek GE, Warfield CA: Clin Orthop Relat Res 1986; 213:216–22
125. Carrera GF: Lumbar facet joint injection in low back pain and sciatica:
Preliminary results. Radiology 1980; 137:665–7
126. Sowa G: Facet-mediated pain. Dis Mon 2005; 51:18–33
127. Dreyer SJ, Dreyfuss PH: Low back pain and the zygapophysial (facet)
joints. Arch Phys Med Rehabil 1996; 17:290–300
128. Dreyfuss PH, Dreyer SJ: Lumbar zygapophysial joint (facet) injections.
Spine J 2003; 3:50S–9S
129. Manchikanti L, Pampati V, Fellows B, Bakhit CE: The diagnostic validity
and therapeutic value of lumbar facet joint nerve blocks with or without adjuvant
agents. Curr Rev Pain 2000; 4:337–44
130. Schwarzer AC, Aprill CN, Derby R, Fortin J, Kine G, Bogduk N: The
false-positive rate of uncontrolled diagnostic blocks of the lumbar zygapophysial
joints. Pain 1994; 58:195–200
131. Manchikanti L, Pampati V, Fellows B, Bakhit CE: Prevalence of lumbar
facet joint pain in chronic low back pain. Pain Physician 1999; 2:59–64
132. Schwarzer AC, Wang SC, Bogduk N, McNaught PJ, Laurent R: Prevalence
and clinical features of lumbar zygapophysial joint pain: A study in an Australian
population with chronic low back pain. Ann Rheum Dis 1995; 54:100–6
612
133. Bogduk N: International Spinal Injection Society guidelines for the performance of spinal injection procedures. Part I: Zygapophysial joint blocks. Clin
J Pain 1997; 13:285–302
134. Newton W, Curtis P, Witt P, Hobler K: Prevalence of subtypes of low
back pain in a defined population. J Fam Pract 1997; 45:331–5
135. Cohen SP, Larkin T, Chang A, Stojanovic M: The causes of false-positive
medial branch blocks in soldiers and retirees. Mil Med 2004; 169:781–6
136. Johnston HM: The cutaneous branches of the posterior primary divisions
of the spinal nerves, and their distribution in the skin. J Anat Physiol 1908;
43:80–91
137. Cohen SP: Sacroiliac joint pain: A comprehensive review of anatomy,
diagnosis and treatment. Anesth Analg 2005; 101:1440–53
138. Bough B, Thakore J, Davies M, Dowling F: Degeneration of the lumbar
facet joints: Arthrography and pathology. J Bone Joint Surg (Br) 1990; 72:275–6
139. Schwarzer AC, Derby R, Aprill CN, Fortin J, Kine G, Bogduk N: The value
of the provocation response in lumbar zygapophyseal joint injections. Clin J Pain
1994; 10:309–13
140. Schwarzer AC, Aprill CN, Bogduk N: The sacroiliac joint in chronic low
back pain. Spine 1995; 20:31–7
141. Slipman CW, Plastaras CT, Palmitier RA, Huston CW, Sterenfeld EB:
Symptom provocation of fluoroscopically guided cervical nerve root stimulation:
Are dynatomal maps identical to dermatomal maps? Spine 1998; 23:2235–42
142. Fairbank JC, Park WM, McCall IW, O’Brien JP: Apophyseal injection of
local anesthetic as a diagnostic aid in primary low-back pain syndromes. Spine
1981; 6:598–605
143. Helbig T, Lee CK: The lumbar facet syndrome. Spine 1988; 13:61–4
144. Carrera GF, Williams AL: Current concepts in evaluation of the lumbar
facet joints. Crit Rev Diagn Imaging 1984; 21:85–104
145. Weishaupt D, Zanetti M, Boos N, Hodler J: MR imaging and CT in
osteoarthritis of the lumbar facet joints. Skeletal Radiol 1999; 28:215–9
146. Leone A, Aulisa L, Tamburrelli F, Lupparelli S, Tartaglione T: The role of
computed tomography and magnetic resonance in assessing degenerative arthropathy of the lumbar articular facets [in Italian]. Radiol Med 1994; 88:547–52
147. Weishaupt D, Zanetti M, Hodler J, Boos N: MR imaging of the lumbar
spine: Prevalence of intervertebral disk extrusion and sequestration, nerve root
compression, end plate abnormalities, and osteoarthritis of the facet joints in
asymptomatic volunteers. Radiology 1998; 209:661–6
148. Wiesel SW, Tsourmas N, Feffer HL, Citrin CM, Patronas N: A study of
computer-assisted tomography: I. The incidence of positive CAT scans in an
asymptomatic group of patients. Spine 1984; 9:549–5
149. Jensen MC, Brant-Zawadzki MN, Obuchowski N, Modic MT, Malkasian D,
Ross JS: Magnetic resonance imaging of the lumbar spine in people without back
pain. N Engl J Med 1994; 331:69–73
150. Dolan AL, Ryan PJ, Arden NK, Stratton R, Wedley JR, Hamann W,
Fogelman I, Gibson T: The value of SPECT scans in identifying back pain likely to
benefit from facet joint injection. Br J Rheum 1996; 35:1269–73
151. Raymond J, Dumas JM, Lisbona R: Nuclear imaging as a screening test for
patients referred for intraarticular facet block. J Can Assoc Radiol 1984; 35:291–2
152. Schwarzer AC, Wang SC, O’Driscoll D, Harrington T, Bogduk N, Laurent
R: The ability of computed tomography to identify a painful zygapophysial joint
in patients with chronic low back pain. Spine 1995; 20:907–12
153. Cohen SP, Hurley RW, Christo PJ, Winkley J, Mohiuddin MM, Stojanovic
MP: Clinical predictors of success and failure for lumbar facet radiofrequency
denervation. Clin J Pain 2007; 23:45–52
154. Kawaguchi Y, Matsuno H, Kanamori M, Ishihara H, Ohmori K, Kimura T:
Radiologic findings of the lumbar spine in patients with rheumatoid arthritis, and
a review of pathologic mechanisms. J Spinal Disord Tech 2003; 16:38–43
155. Kellegren JH: On the distribution of pain arising from deep somatic
structures with charts of segmental pain areas. Clin Sci 1939; 4:35–46
156. Nash TP: Facet joints: Intra-articular steroids or nerve block? Pain Clin
1990; 3:77–82
157. van Kleef M, Barendse GA, Kessels A, Voets HM, Weber WE, de Lange S:
Randomized trial of radiofrequency lumbar facet denervation for chronic low
back pain. Spine 1999; 24:1937–42
158. Gallagher J, Petriccione di Vadi PL, Wedley JR, Hamann W, Ryan P,
Chikanza I, Kirkham B, Price R, Watson MS, Grahame R, Wood S: Radiofrequency
facet joint denervation in the treatment of low back pain: A prospective controlled double-blind study to assess its efficacy. Pain Clinic 1994; 7:193–8
159. Leclaire R, Fortin L, Lambert R, Bergeron YM, Rossignol M: Radiofrequency facet joint denervation in the treatment of low back pain: A placebocontrolled clinical trial to assess efficacy. Spine 2001; 26:1411–7
160. van Wijk RM, Geurts JW, Wynne HJ, Hammink E, Buskens E, Lousberg R,
Knape JT, Groen GJ: Radiofrequency denervation of lumbar facet joints in the
treatment of chronic low back pain: A randomized, double-blind, sham lesioncontrolled trial. Clin J Pain 2005; 21:335–44
161. Greher M, Scharbert G, Kamolz LP, Beck H, Gustorff B, Kirchmair L,
Kapral S: Ultrasound-guided lumbar facet nerve block: A sonoanatomic study of
a new methodological approach. ANESTHESIOLOGY 2004; 100:1242–8
162. Greher M, Kirchmair L, Enna B, Kovacs P, Gustorff B, Kapral S, Moriggl
B: Ultrasound-guided lumbar facet nerve block: Accuracy of a new technique
confirmed by computed tomography. ANESTHESIOLOGY 2004; 101:1195–2000
163. Galiano K, Obwegeser AA, Bodner G, Freund M, Maurer H, Kamelger FS,
Schatzer R, Ploner F: Ultrasound guidance for facet joint injections in the lumbar
spine: A computed tomography-controlled feasibility study. Anesth Analg 2005;
101:579–83
164. Kullmer K, Rompe JD, Lowe A, Herbsthofer B, Eysel P: Ultrasound image
of the lumbar spine and the lumbosacral transition: Ultrasound anatomy and
possibilities for ultrasonically-controlled facet joint infiltration [in German]. Z
Orthop Ihre Grenzgeb 1997; 135:310–4
165. Lord SM, Barnsley L, Bogduk N: The utility of comparative local anesthetic blocks versus placebo-controlled blocks for the diagnosis of cervical
zygapophysial joint pain. Clin J Pain 1995; 11:208–13
166. Hogan QH, Abram SE: Neural blockade for diagnosis and prognosis: A
review. ANESTHESIOLOGY 1997; 86:216–41
167. Manchikanti L, Pampati V, Damron K: The role of placebo and nocebo
effects of perioperative administration of sedatives and opioids in interventional
pain management. Pain Physician 2005; 8:349–55
168. Manchikanti L, Pampati V, Damron KS, McManus CD, Jackson SD, Barnhill RC, Martin JC: The effect of sedation on diagnostic validity of facet joint nerve
blocks: An evaluation to assess similarities in population with involvement in
cervical and lumbar regions. Pain Physician 2006; 1:47–52
169. Cohen SP, Mullings R, Abdi S: The pharmacologic treatment of muscle
pain. ANESTHESIOLOGY 2004; 101:495–526
170. Cucuzzella TR, Delport EG, Kim N, Marley J, Pruitt C, Delport AG: A
survey: Conscious sedation with epidural and zygapophyseal injections: Is it
necessary? Spine J 2006; 6:364–9
171. North RB, Kidd DH, Zahurak M, Piantadosi S: Specificity of diagnostic
nerve blocks: A prospective, randomized study of sciatica due to lumbosacral
spine disease. Pain 1996; 65:77–85
172. Ambroz C, Scott A, Ambroz A, Talbott EO: Chronic low back pain
assessment using surface electromyography. J Occup Environ Med 2000; 42:
660–9
173. Geisser ME, Ranavava M, Haig AJ, Roth RS, Zucker R, Ambroz C, Caruso
M: A meta-analytic review of surface electromyography among persons with low
back pain and normal, healthy controls. J Pain 2005; 6:711–26
174. Browning R, Jackson JL, O’Malley PG: Cyclobenzaprine and back pain: A
meta-analysis. Arch Intern Med 2001; 161:1613–20
175. Foster L, Clapp L, Erickson M, Jabbari B: Botulinum toxin A and chronic
low back pain: A randomized, double-blind study. Neurology 2001; 56:1290–3
176. Ackerman WE, Munir MA, Zhang JM, Ghaleb A: Are diagnostic lumbar
facet injections influenced by pain of muscular origin? Pain Practice 2004;
4:286–91
177. Woolf CJ, McMahon SB: Injury-induced plasticity of the flexor reflex in
chronic decerebrate rats. Neuroscience 1985; 16:395–404
178. Woolf CJ, Wiesenfeld-Hallin Z: The systemic administration of local anaesthetics produces a selective depression of C-afferent fibre evoked activity in
the spinal cord. Pain 1985; 23:361–74
179. Stojanovic MP, Zhou Y, Hord ED, Vallejo R, Cohen SP: Single needle
approach for multiple medial branch blocks: A new technique. Clin J Pain 2003;
19:134–7
180. Stojanovic MP, Dey D, Hord ED, Zhou Y, Cohen SP: A prospective
crossover comparison study of the single-needle and multiple-needle techniques
for facet-joint medial branch block. Reg Anesth Pain Med 2005; 30:484–90
181. Berven S, Tay BB, Colman W, Hu SS: The lumbar zygapophyseal (facet)
joints: A role in the pathogenesis of spinal pain syndromes and degenerative
spondylolisthesis. Semin Neurol 2002; 22:187–95
182. Dreyfuss P, Halbrook B, Pauza K, Joshi A, McLarty J, Bogduk N: Efficacy
and validity of radiofrequency neurotomy for chronic lumbar zygapophysial joint
pain. Spine 2000; 25:1270–7
183. Kornick C, Kramarich SS, Lamer TJ, Sitzman BT: Complications of lumbar
facet radiofrequency denervation. Spine 2004; 29:1352–4
184. Dobrogowski J, Wrzosek A, Wordliczek J: Radiofrequency denervation
with or without addition of pentoxifylline or methylprednisolone for chronic
lumbar zygapophysial joint pain. Pharmacol Rep 2005; 57:475–80
185. Bogduk N, Holmes S: Controlled zygapophysial joint blocks: The travesty
of cost-effectiveness. Pain Med 2000; 1:24–34
186. Geisser ME, Wiggert EA, Haig AJ, Colwell MO: A randomized, controlled
trial of manual therapy and specific adjuvant exercise for chronic low back pain.
Clin J Pain 2005; 21:463–70
187. Sherman KJ, Cherkin DC, Erro J, Miglioretti DL, Deyo R: Comparing yoga,
exercise, and a self-care book for chronic low back pain: A randomized, controlled trial. Ann Intern Med 2005; 143:849–56
188. Maul I, Laubli T, Oliveri M, Krueger H: Long-term effects of supervised
physical training in secondary prevention of low back pain. Eur Spine J 2005;
14:599–611
189. Staal JB, Hlobil H, Twisk JW, Smid T, Koke AJ, van Mechelen W: Graded
activity for low back pain in occupational health care: A randomized, controlled
trial. Ann Intern Med 2004; 140:77–84
190. Williams KA, Petronis J, Smith D, Goodrich D, Wu J, Ravi N, Doyle EJ Jr,
Gregory Juckett R, Munoz Kolar M, Gross R, Steinberg L: Effect of Iyengar yoga
therapy for chronic low back pain. Pain 2005; 115:107–17
191. Andersson GB, Lucente T, Davis AM, Kappler RE, Lipton JA, Leurgans S:
A comparison of osteopathic spinal manipulation with standard care for patients
with low back pain. N Engl J Med 1999; 341:1426–31
192. Giles LG, Muller R: Chronic spinal pain: A randomized clinical trial
comparing medication, acupuncture, and spinal manipulation. Spine 2003; 28:
1490–502
193. Licciardone JC, Stoll ST, Fulda KG, Russo DP, Siu J, Winn W, Swift J Jr:
Osteopathic manipulative treatment for chronic low back pain: A randomized
controlled trial. Spine 2003; 28:1355–62
194. Meng CF, Wang D, Ngeow J, Lao L, Peterson M, Paget S: Acupuncture for
chronic low back pain in older patients: A randomized, controlled trial. Rheumatology 2003; 42:1508–17
195. Tsukayama H, Yamashita H, Amagai H, Tanno Y: Randomised controlled
trial comparing the effectiveness of electroacupuncture and TENS for low back
pain: A preliminary study for a pragmatic trial. Acupunct Med 2002; 20:175–80
196. Kerr DP, Walsh DM, Baxter D: Acupuncture in the management of
chronic low back pain: A blinded randomized controlled trial. Clin J Pain 2003;
19:364–70
197. Brinkhaus B, Witt CM, Jena S, Linde K, Streng A, Wagenpfeil S, Irnich D,
Walther HU, Melchart D, Willich SN: Acupuncture in patients with chronic low
back pain: A randomized controlled trial. Arch Intern Med 2006; 166:450–7
198. Zerbini C, Ozturk ZE, Grifka J, Maini M, Nilganuwong S, Morales R, Hupli
M, Shivaprakash M, Giezek H: Efficacy of etoricoxib 60 mg/day and diclofenac
150 mg/day in reduction of pain and disability in patients with chronic low back
pain: Results of a 4-week, multinational, randomized, double-blind study. Curr
Med Res Opin 2005; 21:2037–49
199. Videman T, Osterman K: Double-blind parallel study of piroxicam versus
indomethacin in the treatment of low back pain. Ann Clin Res 1984; 16:156–60
200. Mens JM: The use of medication in low back pain. Best Pract Res Clin
Rheumatol 2005; 19:609–21
201. Schnitzer TJ, Ferraro A, Hunsche E, Kong SX: A comprehensive review of
clinical trials on the efficacy and safety of drugs for the treatment of low back
pain. J Pain Symptom Manage 2004; 28:72–95
202. Polatin PB, Kinney RK, Gatchel RJ, Lillo E, Mayer TG: Psychiatric illness
and chronic low-back pain: The mind and the spine-which goes first? Spine 1993;
18:66–71
203. Fayad F, Lefevre-Colau MM, Poiraudeau S, Fermanian J, Rannou F, Wlodyka Demaille S, Benyahya R, Revel M: Chronicity, recurrence, and return to
work in low back pain: Common prognostic factors [in French]. Ann Readapt
Med Phys 2004; 47:179–89
204. Lilius G, Laasonen EM, Myllynen P, Harilainen A, Salo L: Lumbar facet
joint syndrome: Significance of non-organic signs. A randomized placebo-controlled clinical study [in French]. Rev Chir Orthop Reparatrice Appar Mot 1989;
75:493–500
205. Lippitt AB: The facet joint and its role in spine pain: Management with
facet joint injections. Spine 1984; 9:746–50
206. Carette S, Marcoux S, Truchon R, Grondin C, Gagnon J, Allard Y, Latulippe M: A controlled trial of corticosteroid injections into facet joints for chronic
low back pain. N Engl J Med 1991; 325:1002–7
207. Lilius G, Laasonen EM, Harilainen A, Gronlund G: Lumbar facet joint
syndrome: A randomised clinical trial. J Bone Joint Surg (Br) 1989; 71:681–4
208. Fuchs S, Erbe T, Fischer HL, Tibesku CO: Intraarticular hyaluronic acid
versus glucocorticoid injections for nonradicular pain in the lumbar spine. J Vasc
Interv Radiol 2005; 16:1493–8
209. Blanchard J, Ramamurthy S, Walsh N, Hoffman J, Schoenfeld L: Intravenous regional sympatholysis: A double-blind comparison of guanethidine, reserpine, and normal saline. J Pain Symptom Manage 1990; 5:357–61
210. Frost FA, Jessen R, Siggaard-Anderson J: A control, double-blind comparison of mepivacaine injection versus saline injection for myofascial pain. Lancet
1980; 1:499–500
211. Price DD, Long S, Wilsey B, Rafii A: Analysis of peak magnitude and
duration of analgesia produced by local anesthetics injected into sympathetic
ganglia of complex regional pain syndrome patients. Clin J Pain 1998; 14:216–26
212. Resnick DK, Choudhri TF, Dailey AT, Groff MW, Khoo L, Matz PG,
Mummaneni P, Watters WC III, Wang J, Walters BC, Hadley MN: American
Association of Neurological Surgeons/Congress of Neurological Surgeons. Guidelines for the performance of fusion procedures for degenerative disease of the
lumbar spine. Part 13: Injection therapies, low-back pain, and lumbar fusion.
J Neurosurg Spine 2005; 2:707–15
213. Bogduk N: A narrative review of intra-articular corticosteroid injections
for low back pain. Pain Med 2005; 6:287–96
214. Slipman CW, Bhat AL, Gilchrist RV, Isaac Z, Chou L, Lenrow DA: A critical
review of the evidence for the use of zygapophysial injections and radiofrequency denervation in the treatment of low back pain. Spine J 2003; 3:310–6
215. Pneumaticos SG, Chatziioannou SN, Hipp JA, Moore WH, Esses SI: Low
back pain: Prediction of short-term outcome of facet joint injection with bone
scintigraphy. Radiology 2006; 238:693–8
216. Holder LE, Machin JL, Asdourian PL, Links JM, Sexton CC: Planar and
high-resolution SPECT bone imaging in the diagnosis of facet syndrome. J Nucl
Med 1995; 36:37–44
217. Lord SM, Barnsley L, Wallis BJ, McDonald GJ, Bogduk N: Percutaneous
radio-frequency neurotomy for chronic cervical zygapophyseal-joint pain. N Engl
J Med 1996; 335:1721–6
218. Cohen SP, Abdi S: Lateral branch blocks as a treatment for sacroiliac joint
pain: A pilot study. Reg Anesth Pain Med 2003; 28:113–9
219. Yin W, Willard F, Carreiro J, Dreyfuss P: Sensory stimulation-guided
613
sacroiliac joint radiofrequency neurotomy: Technique based on neuroanatomy of
the dorsal sacral plexus. Spine 2003; 28:2419–25
220. Barendse GA, van Den Berg SG, Kessels AH, Weber WE, van Kleef M:
Randomized controlled trial of percutaneous intradiscal radiofrequency thermocoagulation for chronic discogenic back pain: Lack of effect from a 90-second 70
C lesion. Spine 2001; 26:287–92
221. Pevzner E, David R, Leitner Y, Pekarsky I, Folman Y, Gepstein R: Pulsed
radiofrequency treatment of severe radicular pain [in Hebrew]. Harefuah 2005;
144:178–80
222. Niemisto L, Kalso E, Malmivaara A, Seitsalo S, Hurri H: Radiofrequency
denervation for neck and back pain: A systematic review of randomized controlled trials. Cochrane Database Syst Rev 2003; 1:CD004058
223. Burton CV: Percutaneous radiofrequency facet denervation. Appl Neurophysiol 1977; 39:80–86
224. Houston JR: A study of subcutaneous rhizolysis in the treatment of
chronic backache. J R Coll Gen Pract 1975; 25:696–7
225. McCulloch JA: Percutaneous radiofrequency lumbar rhizolysis (rhizotomy). Appl Neurophysiol 1976 – 1977; 39:87–96
226. Ogsbury JS, Simon RH, Lehman RA: Facet denervation in the treatment of
low back syndrome. Pain 1977; 3:257–63
227. Oudenhoven RC: The role of laminectomy, facet rhizotomy and epidural
steroids. Spine 1979; 4:145–7
228. Rashbaum RF: Radiofrequency facet denervation. Orthop Clin North Am
1983; 14:569–75
229. Lora J, Long D: So-called facet denervation in the management of intractable back pain. Spine 1976; 1:121–6
230. McCulloch JA, Organ LW: Percutaneous radiofrequency lumbar rhizolysis
(rhizotomy). Can Med Assoc J 1977; 116:30–2
231. Schaerer JP: Radiofrequency facet rhizotomy in the treatment of chronic
neck and low back pain. Int Surg 1978; 63:53–9
232. North RB, Han M, Zahurak M, Kidd DH: Radiofrequency lumbar facet
denervation: Analysis of prognostic factors. Pain 1994; 57:77–83
233. Geurts JW, Van Wijk RM, Stolker RJ, Groen GJ: Efficacy of radiofrequency
procedures for the treatment of spinal pain: A systematic review of randomized
clinical trials. Reg Anesth Pain Med 2001; 26:394–400
234. Lau P, Mercer S, Govind J, Bogduk N: The surgical anatomy of lumbar
medial branch neurotomy (facet denervation). Pain Med 2004; 5:289–98
235. Bogduk N, Macintosh J, Marsland A: Technical limitations to the efficacy
of radiofrequency neurotomy for spinal pain. Neurosurgery 1987; 20:529–34
236. Chua WH, Bogduk N: The surgical anatomy of thoracic facet denervation.
Acta Neurochir 1995; 136:140–4
237. Vinas FC, Zamorano L, Dujovny M, Zhao JZ, Hodgkinson D, Ho KL,
Ausman JI: In vivo and in vitro study of the lesions produced with a computerized radiofrequency system. Stereotact Funct Neurosurg 1992; 58:121–33
238. Buijs EJ, van Wijk RM, Geurts JW, Weeseman RR, Stolker RJ, Groen GG:
Radiofrequency lumbar facet denervation: A comparative study of the reproducibility of lesion size after 2 current radiofrequency techniques. Reg Anesth Pain
Med 2004; 29:400–7
239. Demazumder D, Mirotznik MS, Schwartzman D: Comparison of irrigated
electrode designs for radiofrequency ablation of myocardium. J Interv Card
Electrophysiol 2001; 5:391–400
240. Benzon HT: Epidural steroid injections for low back pain and lumbosacral
radiculopathy. Pain 1986; 24:277–95
241. Quigley MR, Bost J, Maroon JC, Elrifai A, Panahandeh M: Outcome after
microdiscectomy: Results of a prospective single institutional study. Surg Neurol
1998; 49:263–7
242. North RB, Campbell JN, James CS, Conover-Walker MK, Wang H, Piantadosi S, Rybock JD, Long DM: Failed back surgery syndrome: 5-year follow-up in
102 patients undergoing repeated operation. Neurosurgery 1991; 28:685–90
243. Schofferman J, Kine G: Effectiveness of repeated radiofrequency neurotomy for lumbar facet pain. Spine 2004; 29:2471–3
244. Mikeladze G, Espinal R, Finnegan R, Routon J, Martin D: Pulsed radiofrequency application in treatment of chronic zygapophyseal joint pain. Spine J
2003; 360–2
245. Barlocher CB, Krauss JK, Seiler RW: Kryorhizotomy: An alternative technique for lumbar medial branch rhizotomy in lumbar facet syndrome. J Neurosurg 2003; 98 (suppl):14–20
246. Schuster GD: The use of cryoanalgesia in the painful facet syndrome.
J Neurol Orthopaed Surg 1982; 3:271–4
247. Staender M, Maerz U, Tonn JC, Steude U: Computerized tomographyguided kryorhizotomy in 76 patients with lumbar facet syndrome. J Neurosurg
Spine 2005; 3:444–9
248. Brechner T: Percutaneous cryogenic neurolysis of the articular nerve of
Luschka. Reg Anesth 1981; 6:18–22
249. Selby DK, Paris SV: Anatomy of facet joints and its correlation with low
back pain. Contemp Orthop 1981; 312:1097–103
250. Silvers HR: Lumbar percutaneous facet rhizotomy. Spine 1990; 15:36–40
251. Kay J, Findling JW, Raff H: Epidural triamcinolone suppresses the pituitary-adrenal axis in human subjects. Anesth Analg 1994; 79:501–5
252. Ward A, Watson J, Wood P, Dunne C, Kerr D: Glucocorticoid epidural for
sciatica: Metabolic and endocrine sequelae. Rheumatology 2002; 41:68–71
253. Alcock E, Regaard A, Browne J: Facet joint injection: A rare form of
epidural abscess formation. Pain 2003; 103:209–10
614
254. Orpen NM, Birch NC: Delayed presentation of septic arthritis of a lumbar
facet joint after diagnostic facet joint injection. J Spinal Disord Tech 2003; 16:285–7
255. Gaul C, Neundorfer B, Winterholler M: Iatrogenic (para-) spinal abscesses
and meningitis following injection therapy for low back pain. Pain 2005; 116:407–10
256. Goldstone JC, Pennant JH: Spinal anaesthesia following facet joint injection: A report of two cases. Anaesthesia 1987; 42:754–6
257. Cohen SP: Postdural puncture headache and treatment following successful lumbar facet block. Pain Digest 1994; 4:283–4
258. Tzaan WC, Tasker RR: Percutaneous radiofrequency facet rhizotomy:
Experience with 118 procedures and reappraisal of its value. Can J Neurol Sci
2000; 27:125–30
259. Katz SS, Savitz MH: Percutaneous radiofrequency rhizotomy of the lumbar facets. Mount Sinai J Med 1986; 53:523–5
260. Deyo RA, Nachemson A, Mirza SK: Spinal-fusion surgery: The case for
restraint. N Engl J Med 2004; 350:722–6
261. Gibson JN, Waddell G, Grant IC: Surgery for degenerative lumbar spondylosis. Cochrane Database Syst Rev 2000; 3:CD001352
262. Jackson RP: The facet syndrome: Myth or reality? Clin Orthop Relat Res
1992; 279:110–21
263. Esses SI, Botsford DJ, Kostuik JP: The role of external spinal skeletal
fixation in the assessment of low-back disorders. Spine 1989; 14:594–601
264. Esses SI, Moro JK: The value of facet joint blocks in patient selection for
lumbar fusion. Spine 1993; 18:185–90
265. Lovely TJ, Rastogi P: The value of provocative facet blocking as a predictor of success in lumbar spine fusion. J Spinal Disord 1997; 10:512–7
266. Manchikanti L, Pampati V, Fellows B, Baha AG: The inability of the
clinical picture to characterize pain from facet joints. Pain Physician 2000;
3:158–66
267. Manchikanti L, Boswell MV, Singh V, Pampati V, Damron KS, Beyer CD:
Prevalence of facet joint pain in chronic spinal pain of cervical, thoracic, and
lumbar regions. BMC Musculoskelet Disord 2004; 5:15
268. Lynch MC, Taylor JF: Facet joint injection for low back pain: A clinical
study. J Bone Joint Surg (Br) 1986; 1:138–41
269. Marks R: Distribution of pain provoked from lumbar facet joints and
related structures during diagnostic spinal infiltration. Pain 1989; 39:37–40
270. Fukui S, Ohseto K, Shiotani M, Ohno K, Karasawa H, Naganuma Y:
Distribution of referred pain from the lumbar zygapophyseal joints and dorsal
rami. Clin J Pain 1997; 13:303–7
271. Young S, Aprill C, Laslett M: Correlation of clinical examination characteristics with three sources of chronic low back pain. Spine J 2003; 3:460–5
272. Lilius G, Harilainen A, Laasonen EM, Myllynen P: Chronic unilateral
low-back pain: Predictors of outcome of facet joint injections. Spine 1990;
15:780–2
273. Laslett M, Oberg B, Aprill CN, McDonald B: Zygapophysial joint blocks in
chronic low back pain: A test of Revel’s model as a screening test. BMC Musculoskelet Disord 2004; 5:43
274. Laslett M, McDonald B, Aprill CN, Tropp H, Oberg B: Clinical predictors
of screening lumbar zygapophyseal joint blocks: Development of clinical prediction rules. Spine J 2006; 6:370–9
275. Jadad AR, Moore RA, Carroll D, Jenkinson C, Reynolds DJ, Gavaghan DJ,
McQuay HJ: Assessing the quality of randomised clinical trials: Is blinding necessary? Control Clin Trials 1996; 17:1–12
276. Sanders M, Zuurmond WW: Percutaneous intra-articular lumbar facet
joint denervation in the treatment of low back pain: A comparison with
percutaneous extra-articular lumbar facet denervation. Pain Clinic 1999; 11:
329–35
277. Taylor JR, Twomey LT: Age changes in lumbar zygapophyseal joints:
Observations on structure and function. Spine 1986; 11:739–45

(Facet) Joint Pain - pain

Transcription

Similar documents

Endoscopic Facet Joint Denervation (Rhizotomy)

Radiologic imaging of facet joints final

the role of lumbotrain

How to tackle performance issues when implementing high traffic

Postoperative Management And Core Stabilization

The STraighT Leg DeaD LifT

Lumbar Spine - askdrlehman.com

Degenerative Lumbar Spine Disease

a new dimension: DYCS Brieda Cabins